Our Universe Revealed, Part 4: The Color of North

Episode Topic: The Color of North 

Taking us beyond the confines of our own experiences, in their book, The Color of North, Shahir Rizk Ph.D., and Maggie Fink '24 Ph.D., traverse the kingdom of life to uncover the myriad ways that proteins shape us and all organisms on the planet. Inside every cell, a tight-knit community of millions of proteins skillfully contorts into unique shapes to give fireflies their ghostly glow, to enable the octopus to see predators with its skin, and to make humans fall in love. Collectively, proteins orchestrate the intricate relationships within ecosystems and forge the trajectory of life. And yet, nature has exploited just a fraction of their immense potential

Featured Speakers:

• Shahir Rizk Ph.D., Associate Professor of Chemistry and Biochemistry, Indiana University South Bend
• Maggie Fink '24 Ph.D., Adjunct Professor, Indiana University South Bend

Read this episode's recap over on the University of Notre Dame's open online learning community platform, ThinkND: https://go.nd.edu/e6af14.

This podcast is a part of the ThinkND Series titled Our Universe Revealed.

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Transcript

Introduction and Welcome

Speaker 10 0:12

So welcome. Uh, my name is Deb Maher. I'm in the Department of Biology at Indiana University South Bend, and I will serve as the moderator for tonight's talk. the R Universe revealed lecture series includes talks in sciences and the arts, uh, steam for everyone. We feature research and creative work being done in our region, and it's an opportunity for us to be curious about ourselves, our world, and the universe. Um, this is a partnership between the St. Joseph County Public Library who hosts the lecture series, Indiana University, south Bend, and University of Notre Dame. tonight actually is the first time that we're doing a pre-book launch, and this is the perfect place to do it. It's a library and, both of our speakers. Have lots of ties crossing back and forth in different ways between Indiana University, south Bend and the University of Notre Dame. so a little bit about our speakers. Maggie Fink, received her bachelor's degree in biochemistry from Indiana University South Bend in 2020, or sorry, yes. 2018. 2019. Okay, I'm getting close. in 2020, Maggie received a National Science Foundation Graduate Research Fellowship. This is a highly prestigious, uh, national graduate fellowship that recognizes the top graduate students in the country. Maggie completed her PhD in Professor Joshua SROs lab at the University of Notre Dame. Um, she studied how genetics and chemical communication affect bacterial behavior in the environment and also during infections. Um, she's an award-winning scientist, poet, and illustrator. She uses visual arts and storytelling to illustrate biochemical and microbiology concepts in blogs. And she currently co-hosts a podcast called Rust Belt Science. She is a science communication postdoctoral scholar at the University of Notre Dame. She here risk completed his undergraduate degree in biology at Indiana University South Bend. Um, he completed his PhD in biochemistry and protein engineering at Duke University and he did postdoctoral work at the University of Chicago. he's also served in a research position at the Center for Rare and Neglected Diseases at the University of Notre Dame. Um, he's currently an associate professor in chemistry and biochemistry at Indiana University South Bend. You begin to see all the going back and forth. Shahir was the first faculty member at IU South Bend to receive the Kot Troll Scholar Award. Only eight faculty in the entire IU system have ever received this award. The Cultural Scholar Award recognizes outstanding scientists who are dedicated to the combination of education, science, and research. Risk was selected for the res, for the award based on his research using proteins to make nano structures that come together and fall apart, um, in response to some sort of signal. This technique has broad applications from improving drug delivery systems to developing biosensors that detect environmental pollutants. Maggie and Shahir are co-creators of, a science communication workshop for PhD students in early career scientist. And this workshop has been held at universities and conferences across the country. In this workshop, they provide techniques on how to effectively communicate science through writing, um, and how to use art and storytelling to create interest and engage a wider audience. So. Without further ado, let's dive into proteins and see what they tell us about us.

Speaker 2 4:01

Thank you so much.

Speaker 3 4:04

Thank you so much, Deb, for that introduction. As she said, this is actually our first time giving a talk like this. We have an upcoming book that we wrote over the past five years called The Color of North, and it is as somebody very lovely said about it, a love letter to protein. So we're excited to talk a little bit about what we love, proteins and some of the stories that inspire us in our research.

Speaker 4 4:32

This is me 12 years ago. I

Proteins in Everyday Life

Speaker 3 4:35

just had my second baby, Patrick and I had a toddler at the time as well, Peter, who did not come this evening because they were busy doing cool teenager things. Unfortunately. But this was 12 years ago. And at the time, my husband was working second shift at a factory. So three o'clock every afternoon he would leave and I would be home with my newborn and my toddler and we would sit in this chair every afternoon into the evening, especially me and Patrick, my newborn. And I would rock him and I would feed him. And we would sit there and I would struggle through all the things that a young mother struggles through. I don't remember a lot about that time as maybe some of you can re not remember or imagine, but I do remember, so I was sitting in this chair every evening come summertime, a spider appeared in the window, which is off to the side. You can maybe see it in the corner. And I'm generally terrified of spiders. So seeing one, a giant orb weaver, which is a little different than this spider here, but the giant orb weaver, which is pretty common around here. Appear over the window, over your child's crib was quite terrifying. But I was stuck with my newborn, feeding him, rocking him, soothing him to sleep every night. But the spider appeared over and over just as the sun was beginning to set and she'd begin to weave this beautiful web in the window. And soon I began to actually appreciate her company as I was alone with my child. And I'd watch her spin this web every single night, and then as just as it got dark, she would stay right in the center of that web and sit all night. So when I was up feeding at 2:00 AM 5:00 AM there was this beautiful spider and her web that she had built. And as the sun began to rise, she would kind of wake back up and begin to actually eat that entire web back over again. It would be gone and she would disappear for the day. But then again in the evening, she would come back. And this happened over and over again every day, all through the summer months. Come fall. By the time my little newborn was no longer wrinkly and honestly now kind of ugly, uh, he was fat and happy. Four month old, five month old, and spider was no longer. Now it turns out that this spider silk, which we all can probably conjure an I image up in our mind of a web that we've seen, it's made up of these tiny little things called proteins. This protein in particular. Now these proteins are so small, they're about 10,000 times smaller than a period at the end of a sentence, but we can see a spiderweb. So what the spider is actually able to do is inside her body, she has this special kind of organ that these proteins are in, and she can shoot them out of that organ and they start to self-assemble into this long thread that then we can see as spider silk. And she has many different types of spider silk that she can make. It turns out, even within a web, I don't know if you can see super clear. Different parts of the web are made up of different parts, types of silk that require slightly different kinds of proteins, but they're all inside of her. Even the silk that she might use to capture prey or wrap up her babies in an egg sack, all different kinds of silk, but they're all made from proteins. And then every night when she would eat that silk, it would turn back into the building blocks, these proteins that would assemble again the next day into a spider web. It turns out that everything that we do, every living thing needs some type of protein to accomplish every biological function. So all of us have proteins in our body now, right? We think about eating protein, which is technically true. We're eating proteins and they come in all. Shapes, sizes, not technically colors, but all different shapes. This one on the far left here is actually from a carrot. This is called an antifreeze protein. So this protein will interact with water and help prevent that water from forming ice to protect the carrot when it gets cold. There's lots of organisms that have these antifreeze proteins and they all look different than the one the carrot has. In the middle here is actually a protein from a bacterium called staphylococcus aureus, which you may know better as staph, right? We get staph infections, and part of the reason those infections are so nasty is because it makes proteins like this, which are actually toxins that can damage our cells, and you can see size-wise, it's much larger than this carrot protein. So these proteins can come in all kinds of structures, and they are essential. For every single thing that every living thing does here on the right. This is actually two proteins that are kind of bundled up together, but this is keratin. Keratin is what makes our fingernails, our hail, our hair. It's on the scales of different reptiles. It's everywhere. And all of these proteins, these are just the smallest snapshot of the types of proteins that exist in all living things. But if we look inside our own human cell, we can see that proteins are involved in things that happen at the microscopic level. And if you took a biology class at any point in time, you may have been shown the representation of a cell like this. It's quite simple. There is the nucleus. We have our DNA, the mitochondria, the powerhouse of the cell, right? Nice, simple, easy peasy. Unfortunately the cell looks a little bit more like this. This is just showing a little corner of what the inside of a cell looks like. This is an illustration by a cool artist called David Good Cell, who likes to illustrate these, molecular proteins that happen in signs of all kinds of cells, and it's actually quite chaotic if you look at it. There's all kinds of things happening. A lot of these are proteins that are just all smooshed together and all of them are doing something different inside of the cell. You have the outside of the cell right here where some of those proteins are actually inserted inside of that to help interact with things that are going on outside of the cell. If you bring food inside the cell, send waste out. So it's very, very chaotic inside of ourselves. Our cells, no matter what that little diagram shows us that maybe we saw in a biology class and inside of our cells, we actually kind of have our own spider web of sorts. There's these things called microtubules, which you can see here in the green. This is a cell. Inside here is the nucleus where the DNA is, and from that we have these long microtubules that we can see under a microscope. These are kind of basically stained green at this point. We can visualize them. They're not as pretty as an orb weaver's web might be, but it's a web silk inside of our own cells. And yes, these are actually made up of proteins just like spider silk. These microtubules are composed of individual protein parts. One of them is represented here. This is called tubulin because scientists are very creative. Okay? This is called tubulin, and like spider silk. They will assemble into these long strands. These green and blue dots here each represent an individual protein and they can stretch the entire length of the cell. They can disassemble and assemble very, very rapidly. So inside of the cell is not this static, stale environment. Things are constantly moving and changing. Along these microtubules, the cell can actually transport things across. So it's almost like a highway. So they can change the highway at any point in time. And it's all because of these proteins. And when my baby was growing and changing and growing, lots of fat cells and all that kind of stuff, microtubules will play playing a huge role in that as well. In addition to being highways and providing structure to the cell, they actually help the cell divide and make a new cell. So here this is an actual microscopy image, so we can see this happening under a microscope, these dark kind of X looking things. That's the DNA. So there's two sets of DNA here. So the cell is getting ready to divide. The microtubules will grab a hold of that DNA and pull them apart and create a new cell. So from birth, these proteins play a huge role in everything that we do is even something as simple as making a new cell. As we're growing and growing, and just like the spider who weaves this beautiful web out of these proteins, that is essential for her survival. Everything that we do

Speaker 4 13:42

relies on proteins. What is your

Immune System and Memory

Speaker 5 14:01

earliest memory ever? What is the one thing that you can remember as far back as you can remember? Well, this is one of my favorite memories. This is me when I was about. Maybe four years old, a chubby baby. And this is my grandmother. This is my mom. We were at her apartment in Egypt where I grew up. And um, over the summertime, both my parents worked and so they left me with my grandmother. And I had lots of fun there because that's where I learned how to cook. And one of my favorite things to cook to this day is the Nile Tilapia. You can imagine, you can find this fish in the Nile'cause you, if you grow up in Egypt. And a great recipe that I still use to this day uses garlic and lime and salt and cumin. You make a paste for the fish and then you fry it in oil and it's delicious. But I want you to think even farther back than when you were a child like this chubby baby. I want you to think back to when you were just these two cells that Banky talked about. We all started out as one cell and then we split into two cells, and then from there to four and then eight and then 16 and so on. And every time we do that, we have to double our DNA so that each cell can end up with a copy of its own DNA. And so this is generally how it happens. You start out with the parental DNA from what we call a mother cell. And the mother cell gives rise to two daughter cells. And we all know hopefully that DNA is a double helix. Yes, it's a double helix. It's two strands that are wrapped around the way you would take a ladder and twist it around. So you have two strands. And the way that it works is that. You have two of the, the parental strands. One of them ends up in one of the new cells and the other one ends up in the other cell. And then based on those, those are shown as the red or pink ones here. Based on those, we can make new strands so that we double everything and so on. And that's how it goes. Well, hopefully, you know that DNA is made of these letters. We call them nucleotides, but we can think of them as letters. And that's the language of DNA. It's a C, G, and T. Hopefully you've heard of those. Right? And because DNA has is double stranded. There are two strands and one has some letters here. The other one has letters there. And here's the trick. Every time there's an A on one strand, there has to be a T on the other strand, because A pairs with T. And every time there's a G on one strand, there's always gonna be a C on the other strand. And that's how they recognize each other, and that's how they wrap around each other. But every now and then when we're replicating making a replica of the DNA, sometimes mistakes happen. And so take a look at what's happening here. We have a sequence of DNA here, and we have a G on one side and a T on the other side. And we know that that's not correct. And our bodies can recognize that. They can recognize that there's a mismatch because we know that G connects to C and t connects to A, but G and T do not bind to each other, do not match with each other. So there is a mismatch. Our bodies can recognize that. But there's still a question. We just divided our cells. We have one strand that has a G and the other one that has a T. We know that one of them is wrong, but we have to figure out which one came from the mother's cell and which one was made in the daughter's cell. We're gonna make the assumption that the one that came from the mother's cell is the correct one. That's the old one. That's the one we rely on. So we have to be able to remember to keep memory of which strand came from the parent's cell and how do we know that? How do we know which strand came earlier? Which one is the old strand? Well, maybe you have an old pair of jeans like these. This is a beautiful painting that Maggie made of a pair of old jeans. Everybody has their favorite pants or their favorite clothes that they wear, and they've been stained and they've been worn out. So you have these rips and grass stains because the older something is the more modifications it picks up. And DNA is no different. The older DNA will always pick up some modifications, and so that's one way that we can remember which one is the old strand. We can use a protein like this one right here. This protein is called Mute H. Mute H, and it can find these mismatches, but it needs to know which of the two is the old one. And when you look and see this little sphere here, this represents a modification that happened to the old strand. And that's how it recognizes it. This modification is called a methyl group. It's tiny. It's only one carbon long methyl group, just one carbon long. And that's it. And that's all the difference that we can use to tell which one is the old strand and which one is the new one. Now, there are other ways to remember. There are many ways to remember without actually remembering. This is, a picture of the cold virus, the common cold virus. How many of you have ever

Speaker 4 19:44

had a cold before? What happens when we get a cold? We

Speaker 5 19:51

get sick, nobody likes it. And then what does our body do? It reacts. If you have a functioning immune system, many things happen. And one of those things is that our bodies produce proteins. Proteins that are called antibodies. Here's a little sketch of an antibody. It has this characteristic Y shape, and the Y shape is kind of like a pitch for, it finds these foreign proteins that don't belong to us, and they attack them. They bind two of them and they recruit other things and they say, here's the enemy. And then once the infection is gone and we feel better, something else happens. We carry a memory of that infection. In fact, we carry the memory in cells that we call memory cells that patrol our immune system. And if the cell is cells in this case is very, very big. This is just the cell surface right here and on the cell surface, we carry that very same antibody that we use to fight off that infection. And these memory cells are carried deep within our bodies and they patrol until that foreign invader comes back again, and then quickly we can fight against it Again. This is a closeup of the interaction between the antibody and a foreign protein, and you can see how it makes this really nice match of a con contour. It matches the contour of the invading protein, and this is how it recognizes it. It's by shape, complementarity, it can complement the shape, recognizes it, and recognizes that it's different from our proteins. This one in particular is an antibody, very closeup of an antibody. That connects to or finds and neutralizes this protein, which comes from this virus right here. This is the smallpox virus. Now I'm old enough and I grew up in part of the world where I have had the smallpox vaccine. I don't remember when I got it because I was very young. Now, smallpox has since been eradicated because of vaccination, because at some point everybody had immunity. There was enough immunity that the virus just was wiped out. So even though I don't remember getting the vaccine, my body

Speaker 4 22:19

remembers this virus. Our immune system is very, very complex

Speaker 5 22:28

and we may not think that bacteria can remember, but in fact they actually do. This is a bacteria phage. The bacteria Phage is a virus that infects bacteria. This is bacteria's enemy number one. It looks kind of like a spaceship because it kind of acts like a spaceship. It has this landing gear and it uses that landing gear to land on the surface of a bacterial cell. This is tiny. We know that bacteria are tiny, but this is far tinier than bacteria. thousands of times smaller than bacteria. And it lands on the bacteria and it injects its DNA into that bacteria, and then the bacteria all of a sudden turns into a bacteria phage, a virus making machine. That DNA takes over the system of the bacteria. And the bacteria starts making thousands and thousands of these viruses until the bacteria burst, and then those viruses go and infect other ones. It's pretty vicious. It's pretty vicious, and as it turns out. Here is a bacteria phage infecting this bacterial cell and it's injecting its DNA and every now and then, just every now and then a bacteria might survive that infection. And when it does, it can use these proteins, cast one and cast two to cut a piece of that DNA, that viral DNA, and then tuck it away in its own genomic, DNA, along with other pieces. You see the different colors here along with other pieces of DNA that it grabbed from all the other viruses that tried and failed to infect it. So in a way, the bacteria are just keeping a little bit of memory of the past infections, and then what happens when that same virus with that green piece of DNA, we'll call it green piece of DNA, infect the bacteria again. Well, we recognize it because we can compare it to the part that we've kept for memory, and now a protein called CAS nine comes in and chops up that viral DNA and says, that's it. You're not doing anything bad. To me, CAS nine is a really great protein because it can make cuts in DNA and we actually use it. This is a closeup of Cas nine and it's bound to DNA and we can actually use it. Researchers can use it to make very precise cuts in DNA and even fixed mutations that can cause disease, and it's right now being used to cure all sorts of disease from sickle cell to different types of cancer. What about plants? Anybody know this plant? The Venus Fly Trap? This was my venous fly trap and I did a very poor job taking care of her, and she died.

Speaker 4 25:26

I was very upset about it. This is a

Speaker 5 25:32

fascinating plant because it's a plant that eats animals. It eats ants and flies, and the secret to doing that are these little hairs that are inside the leaves. These hairs act as the trigger for the trap. When these hairs are triggered, the trap is set and very quickly the leaves will clamp on that poor animal, that poor insect, and they will digest it. The plant will digest it. Now, you have to make sure that you don't just trigger the trap anytime you have to do it precisely. You have to make sure that there's a real insect there. And so as it turns out, if you touch the hair just once, nothing will happen. You have to touch those hairs twice, and it has to happen within a certain amount of time. That means that the plant has to register that first trigger, keep track of it, and remember it for a short amount of time until a second trigger happens. And this really puzzled scientists for many, many years until some scientists figured it out. And the key was this protein among many other proteins. This is a zoomed in view of a protein known as a calcium channel. And as the name implies, it's a channel where calcium can pass through. And what you're seeing here, these are just calciums flowing through, and it allows calcium to fro flow from one compartment of the cell to another. Every time that hair is triggered, calcium will flood from one side to another, and it's once you have enough calcium, that's when the leaves will trigger shut. Now, one cal, one trigger or one touch of the hair is not enough to get enough calcium. You need two and you need them to happen fairly close to each other. And you can see that here. Hopefully you can see that here over time when you touch the hair, once the calcium levels will go up, but then another mechanism will start to bring that down. Calcium will leak out unless there's another trigger that happens close enough. And what's that going to do? It's going to go above that threshold so that it can close. And once it closes, well now you have an insect that's struggling inside and it's triggering more and more and more. And what happens here, once you reach that next threshold, you get what's known as gene expression that's making more proteins, and it actually makes many proteins, including this protein right here, which is a digestive protein. It's one that will go and start to digest that insect. Now just like this plant has to remember, it has to forget. It can't hold on to that first trigger forever. And that's exactly what happens here. That's where the gray lines are showing because just like calcium will pass through, it will also start to exit. And so just like a plant has to remember, it also has to forget. And sometimes just like we remember,

Genetic Diseases and Mutations

Speaker 4 28:51

we sometimes also have to forget. This is again my sweet baby

Prions and Infectious Proteins

Speaker 3 29:14

toddler, Peter, about 12 years ago, sorry. And my grandfather, Donald Charles Wright, my grandfather, was diagnosed with Alzheimer's disease, which I'm sure everyone in this room has some level of experience with somebody who has Alzheimer's or some form of dementia. And it's really a devastating disease at this time. My grandpa was fine. This is one of the few pictures we have of him with one of his great-grandchildren. But eventually he did start to forget many, many things. He didn't remember who I was, who his own children was, were, but I like this picture'cause you can see, he clearly knows he is with family. And um, Alzheimer's is a devastating disease. But like with most diseases, it turns out it's because something has gone wrong with a protein inside of our body. And in the case of Alzheimer's, we have these proteins called amyloid beta proteins, which you can see here at the top. It's a pretty small looking protein compared to some of the other ones you've seen this evening. It's got these little coil structures and they're in our brains. We don't a hundred percent understand what they do, but they do have some normal biological functions. However, as you get older, you might experience some stressors and a lot of other factors that scientists still don't know that protein unfolds. It loses that coil shape and turns into this structure down here. So instead of looking like little mini staircases, it turns into this kind of long sheet, and you can imagine if you have like a slinky or maybe a spring, it's very difficult to kind of get things to stick to each other that are like springs. There's not a lot of interactions that can happen, but if you have a flat thing interacting with another flat thing, they're gonna start sticking together a lot more. That's exactly what happens in Alzheimer's. This spiral amyloid beta protein turns into this flat one, and those proteins start to stick together and form what we call aggregates. And those are turned into plaques inside the brain, and that's a characteristic of Alzheimer's disease. We don't fully understand how, why, or even how to treat it, but we do know that when we look at the brain of somebody with Alzheimer's, we see these proteins that have basically gone rogue and decided to take on a completely new structure and have started to cause devastation in the brain. And Alzheimer's isn't the only disease that involves proteins. Most diseases that we know involve some type of protein that's gone wrong, and a lot of those are genetic diseases. I think we hear about that in the world, right? Genetic diseases. You can get your DNA tested to see if you're more likely to develop a disease because of something in your DNAA mutation that you might have. What does that actually mean? What does your DNA have to do with a disease? And in biology we have this thing called the central dogma, where essentially we have our DNA, which here talked about, that carries the information, the instructions for how to make all of these proteins that we've been talking about tonight. So all of us have DNA and a lot of that. DNA is gonna be very similar because we need those proteins to do basic things like digest our food. The differences that we have in ourselves are due to changes in the DNA, but those are in inevitably going to lead to some type of difference in a protein. So with a genetic disease, essentially what happens is Shahir talked about the language of DNA. It was four letters, TACG, but there's also a language of proteins. And if we have our DNA, which you can see here at the top, they're paired into groups of three. So each word is three letters, essentially. So for example, TTC that corresponds to, and this I have represented F, but that is corresponds to an amino acid. So proteins are made up of these molecules called amino acids, and there's 20 of them that we can make proteins out of. So the machines will come to the DNA, get the information, take it to the protein making machines and say, this is what we need to make. We need to put an F here, an R here, P, and so on. And those will correspond to different molecules that then assemble into those structures that we've showed you. However, if we get a mutation, which is something changed for in the DNA, in this case, I changed the C to an A. Very, very small change, but that completely changes the word that's being translated into a protein. So instead of putting a P, in this case, a proline is the amino acid, we're going to get a T. Sometimes that's fine. We even if our body isn't able to catch those mistakes and fix them, sometimes those mutations don't really affect the protein and it can continue on as normal. But sometimes even a single mutation like this can totally disrupt the function of a protein. And we've been showing our protein structures basically without these little arms over here, just showing them with these helical structures or sometimes those sheet structures. In reality, what's actually happening is all along the lines of these backbones, there's chemicals that are those amino acids that have different molecules attached to them, and they're gonna be sticking out in different ways. So for example, here we have an amino acid on the end of this helix, and it's gonna be reaching over here and trying to interact with this one. And that might help hold that protein structure together. If we change this amino acid, if there's a mutation and all of a sudden this chain is a lot shorter, that structure might not be the same anymore because we're disrupting how those molecules are interacting with each other. So a genetic mutation, yes, corresponds to something that has gone wrong in the DNA, the instructions got jumbled up, but that instruction that got jumbled up leads to something changing in the protein itself. And proteins, their structure is important for how they function. And if we lose the function of the protein. We're gonna lose the ability for it to do its biological function in our bodies, and that might lead to disease and a lot of times death, inevitably some genetic diseases that we know pretty well. the first one, cystic fibrosis. Has anybody heard of cystic fibrosis? This is a pretty nasty disease. I actually studied a lot about the bacterial infections that happen in cystic fibrosis during my PhD, but basically cystic fibrosis is a mutation in a gene that seems kind of boring. It's not really that interesting of a protein. It's this, like Shahir said, this channel essentially that bridges the outside to the inside of the cell and it allows things to move in and move out so you can get rid of water, get rid of salt, and keep this nice balance between the outside and inside of the cell. You can see this kind of little hinge thing at the bottom that allows the protein to control when and what is coming in and out. A mutation in somebody with cystic fibrosis means that this gait, this part of the protein that's controlling how and when and what comes out is basically locked. So now we can have a, an accumulation of things on either side of the cell and in the case of the lungs, we're gonna have a lot of mucus. That kind of gets stuck and that's what's gonna lead to a lot of the symptoms that we see cystic fibrosis patients with. But it's one mutation in a protein and you completely disrupt the ability for this protein to do its job leading to very severe disease. Some of you may have heard of Bubble Boy from sixties, seventies, I believe there was a movie as well with John Travolta. I think I saw that at some point. and this boy here, bubble Boy, he had what is called severe Combined immunodeficiency Disorder and this disease, basically you have no immune system. So that's why he was forced to live in a bubble literally. And was not able to really interact with anyone in the outside world at all because he had no immune system to protect himself. And again, this disease is caused by a mutation in a single protein. Again, a kind of boring protein that doesn't really do anything that we would think is interesting, but it helps recycle molecules in the cell that can build up, and if they build up too much, it completely disrupts your immune system and you don't have one. So in the case of people who have skids, they lose the ability to clear these things out of your body, and it's just one mutation in your DNA that leads to a protein that can't function. Sickle cell is another one that probably a lot of people have heard of a mutation in the protein or in the DNA that codes for hemoglobin, which is inside of our red blood cells. And it's important for moving oxygen through our bodies. Normally these hemoglobin proteins kind of as the name should suggest, are like globs. They kind of look like big knots and they go in the red blood cell and they help carry the blood, the oxygen throughout all the parts of your body, and they give the red blood cell the shape that it has in sickle cell, that hemoglobin has mutation and it's no longer forming these nice little globs. Instead, it's forming these long chains and not only can it then not do its function of carrying oxygen, it completely changes the shape of the cell, which is where we get that sickle cell shape giving this disease its name. So I think it's important to remember that yes, genetic diseases are changes in our DNA, but the next step then is they are completely changing a protein and its ability to carry out sometimes very simple biological functions that we don't even know are happening inside of our bodies. But there's another kind of disease caused by proteins. I find super interesting, especially now that I'm a microbiologist who studies infectious disease. There are these things called prions, which stands for pro tenacious infectious particle. Again, we're very creative as scientists. So several decades ago, a scientist visited a tribe of people in Papua New Guinea, the foray people, and he went there to study them because they had this weird disease that nobody could figure out what was happening. It was very similar to Alzheimer's in a lot of ways. People would lose their sense of self, not remember anything, and they actually called it laughing sickness because essentially they would kind of go crazy and then eventually die. What was interesting about this though is it didn't just affect old people. They were seeing this disease show up in children as well, so it wasn't like Alzheimer's. Something was happening that was not specific to age. That didn't just happen when you got older. Excuse me. So he studied these people for a long time, couldn't figure it out, and it would sometimes take years and years for people to start showing these sickness, even if they'd been exposed to somebody else with it before. He noticed that these people participated in a cannibalistic ritual where after somebody passed away, they would eat their body as a sign of honor and remembering them. And what was interesting is that the women and children would eat the brain, and those were the people who were most likely to be affected by this disease. So they thought maybe there was some bacteria or virus that resided in the brain that was causing this disease. But typically with a bacterial infection or a viral infection, you might get a fever, you might get aches and chills, and you get sick pretty quickly after you're exposed to it. But like I said, it would be years before people would show signs of sickness. There was no fever, no other signs until they would start to mentally decline. So many, many years of research into these people and many other scientists got involved as well, as you might have guessed, discovered that it was actually a protein. Very similar again to what we see in Alzheimer's. This protein here, which they called a PreOn, that was actually able to be passed on from person to person. And like Alzheimer's, it starts off normally shaped. It's got its normal structure with these helices and then it for some reason unfolds and has those long sheets instead, and they begin to stick together and they form these large aggregates that can really disrupt the brain tissue. And eventually you die. And you can actually see some of those in some brain samples here. And you may have actually heard of this disease before. Mad Cow disease is a PreOn based disease. We've had several outbreaks in the past decades, from people eating infected beef. They also see this in sheep, and you can get sick just from ingesting it. And even if you have a very healthy PreOn protein in your brain, if you inject ingest one that's already been misfolded and changed into the shape, that one will start forcing all of your normal proteins to unfold and form those aggregates. So in that way, it's infectious, which is truly marvelous that something that is not alive like a protein can be in an infectious material and we're not likely to die from a prion disease. Right? It's very, very rare and it's very well controlled at this point in time. But we will likely die from some type of protein that has gone rogue. And I would like to read. Just a short excerpt from our book, about my grandfather, which you can see here with me as a baby. This time my grandpa died from Alzheimer's. I have a picture with him, of him, with me as a baby. My uncle is on the couch and my grandpa is holding me on the floor. Nobody looks ready to have their picture taken, but nonetheless, the camera captures everything about my grandpa and our time together. It was easy and casual. He was a quiet man who always loved to tell about his time on the railroad. I would tell him about my boy crushes and he would always respond in his subtle southern accent. Well, isn't that nice darling? And give me a big squeeze. My grandpa ran a car mechanic shop outta the garage right electric, so he could be close to his family. I was always proud to see my last name on a sign when we visited. I would pick up colorful cut wires in the driveway on my way up to the front door and keep them in my pocket to admire on the way home. My grandpa would come in through the back door, all covered in oil and sweat when it was time to eat, with his strong broad chest and his white shirt and jeans, and the rugged lines etched into his face. From years of hard work, he looked like he could have walked out of a James Dean movie. He called us All Darling as we fought over who would get to sit next to him. I was able to visit a few years before he died. My parents, my sister, and aunts and uncles and a few cousins all made the trip to Anderson, Indiana. I arrived with my parents and sister at the tiny house on School Street before everyone else. I quickly went to be with him. He was in a rocking chair in the middle of the room with his favorite music, old Coral hymns, playing loudly on the speaker that my aunt and dad had gotten for him. He smiled when I walked in while looky there, such a fine lady, he said. I sat down across from him and asked him how he was doing. He told me he liked his music. I showed him pictures of my cats and commented on his new sweatpants. We sat together for a long time. As everyone trickled in, he smiled, but he didn't know us All he said to me was, we are connected and we all belong to each other. I sat next to him at lunch, cutting up his food, helping him bring a fork to his mouth. I snuck him the extra piece of cake he asked for. I knew it was likely the last time I would be with him like this, sitting at the dining table, the door to his garage right next to us. His favorite hymns playing in the background, a granddaughter feeding her grandfather. Later, when it was time to to leave, I kneeled down next to where he sat in his chair, his worn Bible on the table next to him. I held his hand and asked him if he remembered me. No response. I am Maggie, your granddaughter, and I love you so much. In a tiny bit of clarity. He smiled again and laughed a bit embarrassed. Of course, darling, I knew it, but I didn't know it. And I love you too. Our bodies will stop functioning one way or another. We cannot cheat death. But as we learn more and more about the great symphony of proteins that make us who we are, we can better understand ourselves and the world around

Speaker 4 46:15

us. This is Professor Gretchen

Understanding Enzymes and Their Importance

Speaker 5 46:37

Anderson. She worked at Indiana University, south Bend, and was my colleague. she absolutely hated bananas. She thought they were disgusting and they smelled really bad. She was right. She says, ironically, Gretchen really loved this stinky creature called Alese Fal. You can imagine why it's called Alese Fal. Well. This is a soil bacteria. It's a bacteria that's find found in soil, but in a very special kind of soil. You can find it in soils where there was a lot of pesticides used, especially pesticides based on arsenic. You may have heard of arsenic and you say, why would anyone want to do that? Well, we don't use it anymore, but for a long time, arsenic was used as a pesticide and it left a lot of fields empty because after repeated use, it would pretty much kill everything. Pretty much, except for this bacteria right here, alese fecal. You see, this bacteria actually loves arsenic. In fact, it eats arsenic for breakfast, as you could say. And as much as Gretchen hated bananas, aegis, fecals, just loved arsenic. And there are many different forms of arsenic. These are the two major forms. One that has three oxygens around it that we call arsonite, and one that has four oxygens around it that we call arsenate. And this bacteria was able to convert arsonite to arsenate. Arsonite is a much more toxic form of arsenic than arsenate is. And in a way, this bacteria was making something that's more toxic, a little less toxic, still quite toxic. And the bacteria was able to do that because of this protein right here called arsonite oxidase. Arsonite oxidase is a protein. It's also an enzyme. It's also

Speaker 4 48:43

an enzyme. You may have heard of enzymes

Speaker 5 48:47

before. Have you heard of

Speaker 4 48:48

enzymes before? What are

Speaker 5 48:51

enzymes? I love food and I love bread. I love bread so much, uh, that I could probably just eat bread and survive on bread forever. And what happens when we eat bread? Well, if we look at the structure of bread or the main component of bread, which is starch, we see that it's made of these long chains, either unbranched or branched chains of glucose. We love glucose. It's our blood sugar. It's what we crave, and every time we eat starch, we use our enzymes to digest it and get these glucose subunits that we can then share with the rest of our body so that we can grow or move or kick a soccer ball or do whatever it is that we do. Now, enzymes make this reaction go really, really fast because without an enzyme, this reaction just cutting off one of these glucose would take about 20 million years. Add a pinch of an enzyme like this one called maltase. Maltase is one of these enzymes, and the reaction happens in 0.08 seconds, 0.008 seconds. I missed the zero there, which basically says that this enzyme can do this reaction about 120 or 130 times. Every time you say one Mississippi, this is an incredible rate acceleration. You're taking something that would take about 20 million years, give or take. Give or take, right? We ha I haven't measured that'cause I'm not that old, but give or take takes about 20 million years and now this enzyme can do it in far less than a second. And if you look at the rate acceleration, it's about 70. Quadrillion times, 70 quadrillion times. That's how amazing enzymes are. I don't know about you, but I don't wanna wait 20 million years to digest my bread. Enzymes are amazing and like arsonite oxidase that Gretchen studied, enzymes do amazing things because they are nature's catalysts. A catalyst is something that makes a reaction go faster. A spontaneous reaction that would happen anyway but might take 20 million years. It can make it happen in a fraction of a second. That's what a catalyst does. And enzymes are nature's catalysts. They are biology catalysts, and in fact, they have changed the face of the earth many, many times. And this is the story of trees. About 300 million years ago were told that. Trees were not really trees. Most plants were about waist high. It was mostly ferns and shrubs. They couldn't really grow very big. And then something happened and eventually one of these enzymes, this is one of the many enzymes that eventually happened to be started putting together carbons into these rings and made this new structure. And the structure is called lignin, which is the main component of wood and bark. And now all of a sudden, these croy little twigs, the tiny little ferns, now we're able to make this new biomaterial called wood and bark, and then all of a sudden they could grow to be giants. huge trees. And it sparked an entire era called the carbon ferous era, because these trees were just taking carbon dioxide from the air and storing it into these carbon. rings right here. And they just kept growing bigger and bigger and bigger, and they just spread everywhere. And then they died. And as it turns out, nature had made a new material using these enzymes, but it hasn't, hadn't really figured out yet how to break them down. They made something that was not biodegradable at all, because nothing could eat that wood. Nothing could break it down. And this went on for about 30 million years or so. And the trees would grow big and die and then pile on top of each other and then push each other down. And the weight was immense and they would get buried. And then today we find them in coal. That is fossil fuel. That's mostly what coal is, is these trees from the carbon Ferous era where they just collected so much carbon dioxide from the air because of these enzymes. And for 30 million years, nothing happened until 30 million years later, a new enzyme, a new set of enzymes came about from fungi and bacteria that were able to break down that wood. And now when a tree dies, it doesn't just get buried. Other enzymes from other organisms will eat it and break it down and return that carbon back to the rest of the world. Great story. But why do we care? You may have heard of penicillin. You may have taken penicillin. You might be allergic to penicillin. What is penicillin? It's an antibiotic. It's an antibiotic. It's something that you take if you have a bacterial infection, and it will help stop the bacteria from growing. And there's a reason for that because penicillin. Can stop a special enzyme that the bacteria use to build their cell wall. We don't have a cell wall. Humans don't have a cell wall. But other things like bacteria and fungi have cell walls, so are plants, and there's an enzyme that helps the bacteria build a cell wall. So every time they need to divide, they need to make a bigger wall so that they can expand and make more. And the penicillin just jams that enzyme, it binds to it, and it jams it, and it stops it from growing. And then our immune system can take over and fight those bacteria. Same thing with HIV. This is the virus that causes age, the human immunodeficiency virus. This is an enzyme from this virus. This enzyme is called the HIV protease. It helps the virus make more of itself when it infects an individual and we can design. These molecules that can bind right in the middle of that enzyme and jam it and stop it from actually functioning and slow down the proliferation and the reproduction of the virus. So, but so enzymes are very, very important in making medicines because if we know how to inhibit them, we can stop viruses and bacteria from growing and even things like cancers. How do they work? How do enzymes make things go so fast? Well, I wish I would've come up with this drawing, but I didn't. I got this from the internet, and this is a really nice illustration of how it works. You have some frogs over here. These are the reactants. This is the initial molecule and an enzyme wants to convert it to another molecule, to a product. But there is a barrier right here. These frogs are trying to jump over. How likely are they to make it? Maybe one, maybe two will make it eventually. They just have to keep trying a lot. And what does the enzyme actually do? All it's doing is that it's removing that barrier. It's lowering the barrier for the reaction to take place. And that's how a catalyst works. It lowers the barrier for a reaction to take place. This is Gretchen again. Gretchen was not only my, my colleague, but she was also my mentor. And this is my picture when, uh, when I was graduating from college and, uh, let's see, Gretchen died in 2019 and in her funeral, nobody really talked about her scientific discoveries. Nobody talked about alig callus or arsonite oxidase or anything that she did. Everybody talked about how she was a catalyst in their life. Have she lowered barriers for success? We all know people who are catalysts in our lives, who work very much like enzymes, who lower barriers for success. And all of us are gonna die one day and one day some enzyme is gonna break us down into smaller things that our enzymes were used to build up. I hope you enjoyed our stories today. Uh, you can find all these stories in our book that is just coming out next month. Uh, you can pre-order it through this link. some of you may have gotten a card when you walked in that has a QR code. I also encourage you to check out our podcast, Russ Belt Science. It is pretty laid back, just conversations with scientists and sometimes just conversations between the two of us, Maggie, and myself, and we're very grateful for all the funding. Especially from the IUSB College of Arts and Sciences. Thank you so much, and the Notre Dame College of Sciences. This is really a wonderful collaboration between the two universities here in town. We also have had a lot of really great support from the Burs Welcome Fund and from the Research Corporation for Science Advancement and the National Science Foundation. I really want to thank you for being here today. There are many, many things that you could have done, but you chose to be here, so thank you.

Speaker 4 59:18

Why, why are there mutations? Why

Speaker 5 59:25

are there mutations? Oh, that's a great question. That is a really good question. Do you wanna take this one? You wanna, okay. All right. Mutations are a natural part of life. mutations happen all the time because our, the enzymes that make our DNA, and not just our DNA, but bacteria, or when they divide, every time you do something, you're gonna make a mistake. And sometimes these mistakes can be deadly, and sometimes these mistakes can give you an advantage. So you don't want to be perfect, because if you're perfect, you'll never change. And so, you know, and nobody likes that. Nobody likes that. So there is a little bit of that. You know, the making mistakes every time you copy DNA is not always a bad thing. Sometimes it is, and a lot of genetic mutations come from that. But also mutations don't just happen from, every time you double your DNA, that is one way that they can happen. But they can also happen from environmental aspects. So things that are carcinogens, you may have heard of the term carcinogens are things that cause mutations. So smoking can can make mutations more happen, more common. Now, again, we always have these proteins that are watching out for us, that are trying to fix mutations as they see them happen in many, many different ways. We only talked about just a handful of them today, but there are so many that are out there watching out for us. So sometimes mutations can be good. Most of the time they're not. A lot of times it happens when we're cells, our cells are dividing, but sometimes it happens just from the environment being exposed to the sun or a carcinogen or any kind of harmful chemical. Does that answer your question? Okay. Good

Speaker 4 1:01:10

turn.

Speaker 2 1:01:12

First of all, thank you for those pictures of Gretchen. It's lovely to see her up there. And a lot of your drawings of the proteins, there were arrows built in. Are those arrows, I mean, I assume they're not actually, you're not seeing arrows, but are they indicative of something?

Speaker 4 1:01:38

Oh gosh.

Speaker 3 1:01:40

He's more of the protein structure bio, and I think that's,

Speaker 5 1:01:43

well, I, I mean, you talked about the sequence, right? You talked about the sequence, how it's, you can think of them as letters in a row. Of course, they're chemicals that are connected together. We just give them letters. And, the arrows tell us where the protein begins and which way it's moving, because there is what we define as a beginning and an end. There's a chemical beginning, there is a chemical end. And it just so happens the way that proteins are made, they're made from one end to another every time they're being made. one is called the end terminus, the other one is the c terminus. Right? It's just the technical term and the way that they are arranged you, it's almost like always writing from right to left in some languages or from left to right in another language. all of biology does it one way, in one way only, and it's always from the N to the C, the nitrogen side to the carbon side. it, that, that has meaning. But, so it tells you about the directionality of the chain because it is a chain. And if you were to pull on one end and just straighten it out, it would be one string of letters. That's another representation, be a linear sequence. And all the arrows would, would point from the beginning to the end.

Speaker 4 1:02:54

Yeah. Yes. What does the book title come? Oh, you have to do that. I already talked you much. Okay. I'll answer

Speaker 3 1:03:08

that one. Yes. Um, so there is a protein that migratory birds have in their eyes that actually allows them to see the magnetic fields that doesn't, C isn't, doesn't necessarily mean the exact same thing that we think it does. We don't really know what they see, but they're able to sense where the magnetic field is when they're doing their migratory pad patterns. And that protein is very similar to the proteins in our eyes, that we actually can detect colors and things like that. So. We don't know what north actually looks like, but we do know that birds, for example, can detect that magnetic field and through their eyes and the

Speaker 4 1:03:48

proteins involved in that. Yes. I have a

Speaker 8 1:03:55

question, but it's not really related to this all the way. Uh, Dr. I noticed that you have a molecule tattoo. What is the molecule that you have?

Speaker 3 1:04:04

I, I'm always gonna be happy to share this. So this molecule here, is called PQS. It stands for Pseudomonas Quorum Sensing Signal. So Pseudomonas Gin is a bacterium that I studied during my thesis work. And this molecule, um, is the one I studied in particular, pseudomonas uses a protein to make this molecule, and this is actually how it can communicate with other pseudomonas bacteria and say, Hey, we're all here. And then they'll all start behaving the same way. So this is basically how they communicate with each other. So, PQS.

Speaker 8 1:04:39

Thank you.

Speaker 4 1:04:43

Yes.

Speaker 8 1:04:44

as a non-scientist, I really appreciate your storytelling and how you're sort of humanizing these, what I think must be a very complicated processes. Um, how did you design on the audience for the book? How did you pitch it? Like, are you thinking about, students or

Speaker 6 1:05:02

do this one, or,

Speaker 8 1:05:03

I I

Speaker 3 1:05:04

think we can probably both answer it. Yeah.

Speaker 4 1:05:06

go ahead.

Speaker 3 1:05:06

We both really love science. I hope you can tell. And we also want non-scientists to care about science and to not be afraid of science. Right. You said it seems complicated. It's complicated, but that's what we like to do. But that doesn't mean that it should stay complicated. This information should be shared with anybody who wants to know it. And so that was before we even started writing this book. This was a driving force. As scientists, we feel like it is our duty to make sure that people who don't have scientific training can still understand information like this. we also were really inspired by other scientists who did similar types of storytelling. So if anybody has not read the book, braiding Sweetgrass, um, by Robin Wal Kimer, that was a huge inspiration for us as well. She uses a lot of storytelling to talk about scientific concepts. and so we really, our audience was our friends and family that exist outside of our research lives that we've tried to talk to about science and have found it difficult sometimes. So, uh, we felt it was our duty to learn how to be better sci scientific storytellers to anybody who wanted to learn more about science, no matter how much scientific training they'd had. And we're humans, we're storytellers. So that seems to be a really effective way. To bring people into our world of research and help people feel empowered to seek out information and not be intimidated by the fact that this is what we do every day. It's just what we do every day. There's nothing extra special about it. So,

Speaker 6 1:06:36

yeah. I have, yeah, exactly. It's yes what she said,

Speaker 5 1:06:42

but I I just, can I just add just one thing? It really comes from a place of joy because when we first saw these really crazy structures of proteins, I mean, look at this. it's beautiful. It looked like abstract art and, but it's, it looks like something that's out of this world, but it is actually something from this world, and that's what's really fascinating about it. It's, it just takes on these amazing shapes. And that's, that was also the art component of the book. So maybe something that I failed to mention is that the book also contains a lot of these drawings. Not everything that you've seen here, but this drawing is one of the drawings that are, that's in the book to illustrate just the kind of, the three dimensionality of these, these molecules. and it's just something that always brought us joy and we felt like we should just share it with everybody. And you don't need to take seven and a half college classes in chemistry or whatever it is that we take, just so that you could get to learn about proteins. We wanted to make it more approachable and just kind of, lower the barriers, if you will. Yes, sir. does CRISPR work into any of your work at all? No, I don't work with CRISPR directly. As it turns out, there are actually many different ways to edit genes. Now, CRISPR just happens to be one of the more famous ones, but I have a lot of friends and colleagues who are using it to actually do a lot of gene editing, where they can use this amazing protein or different types of proteins that target, uh, uh, specific parts of DNA. They find that sequence that, you know, we want or we can program them to do. They go in and they cut it out. And then if you provide that, that you know, a good copy if you will, then other proteins will come in and fix that, hopefully, most of the time. Again, this is kind of, uh, my understanding of it because it's not my direct field, Doug.

Speaker 9 1:08:34

So I just wanna applaud you, for this work, making science. Hardcore. It's always been a tough thing. Me because k12 for example, how do we do this k12? Okay, yeah. We to know the structure of cell, right? Mytosis, myosis and all things, but that really for the most of our pelvic doesn't work. So how do we do stuff like that? Or, you know, through 12 and making science accessible to them because we really have not done a really good job communicating the importance of science and how science is done. And, you know, the beauty and joy of science in our K through 12,

Speaker 3 1:09:14

as a mother of two, middle school, almost high school boys, I don't know if I have the best perspective,'cause they're kind of sick of science in my house. They're, that's why they're not here today. But I, you know, as a scientist, I have tried to go to K through 12 schools and participate in science fair judging and actually talk to the kids about, and talk to teachers as well. Say this is not just, um. Teaching facts about science, we're actually trying to get them to think like a scientist and ask a question and be curious. and there's not really a wrong answer when you're asking a question. Uh, and just to keep kids curious, I think you kind of beat the curiosity out of them when they come. You know, my kids just memorizing all type of scientific facts right now and it gets really boring and I, you know, you do have to learn so much information to understand science it feels like. But then what's missing, even as scientists who have now completed PhDs and are doing research, the curiosity can still not be there'cause you're trying to follow a specific path. So I usually tell teachers when I'm talking to them, just let your kids be curious and ask questions, even if it's not directly related to the fact that you need them to memorize. But, I would take data, I did a lot of microscopy. I'd take those images home to my kids and be like, what do you see? What do you think's going on? Even though they had no frame of reference for. I was doing and let them just explore the world of science. And I think going in and teaching science from a question driven perspective, even at that young age, is really gonna help people understand what science is and what it is not. It is not just memorizing a bunch of facts. it is, science is constantly changing. I think that's another thing. It's, we were joking before in 20 years, probably most of what we showed will be irrelevant or proven to be wrong or totally different.'cause science is not just this textbook that we all have to memorize, but, my preferred audience is adults, not children, because I have to live with them. yeah. But I, that's what I, that's my advice is to teachers who do it is just let the kids stay curious and don't make them lose that sense of wonder. And even as adults, you should, I'm always happy when people ask questions.'cause as you stay curious. And that's what we have to do every day as scientists. I don't know if you have any

Speaker 5 1:11:29

I I, I agree completely. I just want to add a little bit of that human aspect of it too. And I think just the perception of what is a scientist, and I think the perception in general, again, I'm sure some people might disagree with me, the perception of a scientist, someone who just knows a lot of things as opposed to someone who can be creative or who can speak or write or imagine or draw or paint. But we know that the vast majority of Nobel Prize winning scientists had a very serious artistic endeavor going on in their life, whether they were authors or poets or, you know, painters, that they go hand in hand. And I feel like just kind of removing art from the sciences has kind of, you know, it siloed us and it really gave the wrong impression about who we are as scientists. I'm not saying that all scientists are artists or have to be artists, but we have to remind everybody that. We are scientists because we are creative. We have to, you know, everything that's ever been invented had to be imagined at, at some point, right? Or to have a use for it. And that comes from creativity. But unfortunately, because when you bring in somebody into the science and you say, here's a bunch of equations, here's what carbon is, here's the periodic table. And they don't understand the beauty and the creativity of the periodic table and what it took to actually make it. And even when we teach them the history behind it, it's just a bunch of dead old white dudes and they don't know any. And it's, it's challenging. But at the same time, what we're doing is that we're just driving creativity away from science. And I don't want that. Right. I'm very envious of my creative writing. Fridays know what I

Speaker 9 1:13:04

say. Someone who ate eats a banana every day. I could attest it. Gretchen hate it.

Speaker 5 1:13:09

Oh yes, absolutely. Absolutely. She did. Yes, she absolutely did. So I, this is why I am really happy to be in the College of Arts and Sciences. This is really very near and dear to my heart. So. Because they belong together. Edwin, do you have a question? Yeah,

Speaker 10 1:13:26

a question about like the, how do you guys get like those, like I know you guys are able to like, draw out the proteins the way you guys did it. How do you guys like get to that point when you guys can like, draw Yeah.

Concluding Remarks and Future Events

Speaker 5 1:13:35

How, how, how do you get to, to draw? Okay. So lemme tell you where these structures come from. Right? So a lot of these structures took scientists years and months and, you know, sweat and tears and, and lots of crying to actually figure out what the structures are. Because proteins are tiny, we can't even see them under the microscope. Only when they make these long polymers like microtubules can you really get to maybe see them. But these structures you have to really work very, you know, under very difficult conditions where you're shooting them with x-rays and sometimes it just blows them apart and you don't actually get a structure. And even after you shoot them with x-rays, you have to do a lot of data analysis to actually get to the structure. You can use other techniques, but that's the most common way. But the wonderful thing about it is that every single protein structure that's ever been determined, has ever been known as far as we know, is deposited and it's publicly available. So any one of you can go to the protein data bank, I highly encourage you to do that. The protein data bank, they usually have the molecule of the month, which is pretty cool. Yeah. Molecule of the month. So you can click on it and you can click on the structure and actually move it around in 3D and see how three dimensional it is. And so we, we look at a protein that we like and then we just start sketching it. And, you know, it takes a little bit to kind of get, get in the habit of drawing. And this is something I want to credit, Dr. Kelsey, for, because she has really. Thank you for the inspiration, Kelsey, back here. Shout out to Kelsey, uh, about just making art every day. I'm terrible at making art every day. I don't do it every day. Uh, but also I'm taking a printmaking class with Bill. Bill Tolo is here. So all these amazing people in our lives who are really pushing us to make art and to really look at science from an artistic point of view. If you wanna draw proteins, just start with something simple, a small, a small one. Just start drawing it. You'll get better because you can get better at art just like anything else. I don't know if that was your

Speaker 6 1:15:35

question, but

Speaker 2 1:15:37

yes,

1:15:37

definitely

Speaker 2 1:15:37

shout out to all

Speaker 6 1:15:38

these wonderful people.

Speaker 2 1:15:40

Alright, why don't we thank them

Speaker 10 1:15:51

And I wanna thank you for coming out tonight. So our, in May on Monday, May 5th, we'll have our last, our Universe revealed lecture series for the spring. we're gonna be going to Africa, sort of, to think about baboons. So, Beth Archie, studies the social life of baboons and, and how it affects their risk of their ability to survive. so that's coming up Monday, May 5th. Notice that it's a Monday, May 5th 6:30 PM same time, same place. and I wanna thank you so much for coming out tonight. You can view past talks, by going to our universe Reveal Notre Dame. We have a YouTube channel, and this talk will be up in probably a couple of weeks and five days, five days. And I wanna thank Steve to, who has been recording this and creating that repository for everybody. So thank you.