How Allelic Variants improve the fight against Chronic Virus Infection (ft. Dr. Robin Orozco)

Maria Losito:  Welcome to Interview with a Biologist. I'm your host, Maria Losito, and I'm joined today by Dr. Robin Orozco, who is assistant professor with the Department of Molecular Biosciences at the University of Kansas. How are you doing today?

Robin Orozco: Good. Thanks for having me, Maria. Yeah, I'm enjoying the warmer weather we're starting to have here.

Maria Losito: It's been so nice. I'm hoping that the snow melts off because I'm getting really tired of that like the salt, or the sort of sand-snow?

Robin Orozco: Yes, I agree.

Maria Losito: Not the prettiest.

Maria Losito: So, you are a faculty member here at KU, would you mind telling us a bit about the classes you teach?

Robin Orozco: Yeah, so I teach the undergraduate Immunology class, Biology 503. I teach the fall section of the class, and Dr. Dyan Morgan teaches the spring section of the class. And then every other spring, I teach the graduate immunology class in the molecular biosciences department, which is primarily graduate students, where it's a little bit more paper based and literature-based type class and then I lead some seminar classes, but mostly it's all focused on immunology, which is also what my research.

Maria Losito: Is this one of the spring semesters where you're teaching graduate students?

Robin Orozco: It is not so I taught last spring semester, so it will be spring of 2025. So next time I teach Graduate Immunology it will be spring of 2027.

Maria Losito: Well grad students, that's a class for you to take next year, so keep an eye out.

Robin Orozco: Absolutely.

Maria Losito: You mentioned that you work on immunology, can you go deeper into what your lab research is?

Robin Orozco: I think before I get into the specific question, I'm going to set up the problem. When we think about immunology and the immune system, it's made up of many different cell types and those cell types have to work together to protect us from pathogens like viruses or certain bacteria, or fungi, as well as help not have cancer develop in our bodies as well.

When we think about these cells coming together and they have their different roles, like a community and a community have different jobs and roles, and they have to communicate with each other to enact this kind of complex function, to protect ourselves. I'm really interested in how those cells are actually communicating with each other and functioning together, and how the genes in those cells and the genetic differences between people change those cells functions and how they communicate.

To do this, we study an allelic variant or a mutation energy in called PTPN22. It is expressed only in immune cells when it comes to humans and mice, and it is an immune regulatory gene. So, it really changes how immune cells function and the mutation we study is present in about 5 to 15% of the North American population.

It’s pretty prevalent and if people have this mutation, they're more likely to develop an autoimmune disease, which is not what we think of as a good thing or a benefit. But the mutation is present at a pretty high level and so this is a bit of a conundrum when we think about it evolutionarily and so my lab tries to understand is, is there a benefit for this allele? And is that based on how the immune cells are functioning and communicating?

What we do is again, we really study this gene and it's allele, and we study it in the context of virus infections and cancers and we've been able to show that if we have this mutation with a mouse model to do this, there is protection against some viruses as well as cancers. Then we're trying to figure out the fundamental immunology behind that.

Maria Losito: That's awesome, so cool. I guess this is just a Maria question, because I'm fascinated by the genetic ancestry of things, do you happen to know if there is a specific area that this gene originated in and then came to America, or was it truly North American based gene?

Robin Orozco: In terms of where this mutation first arose, we don't know that. There's a new anthropologist at KU, Obed Garcia -- we are meeting next week, Obed, if you're listening to this-- that's a question I actually plan on posing to him because he has the knowledge and the skill set to try to answer questions like that.

We're going to see if we can form a collaboration with that but in present day, we can look at global population and notice where presence of this mutation is highest and see there is a geographical distribution, Northern European and Finnish populations have the highest percentage of this population. There’re some reports reporting 20% of the population or 1 in 5 people have this mutation. 

If we look at populations that are more equatorially close, if we look at different African populations or South Asian populations, this mutation is almost not present at all. That indicates that there is some sort of selection, whether that's neutral, positive or negative, we don't know, but there is something biasing this and whether that's due to specific kinds of disease outbreak that occurred in different populations or where the mutation originally popped up. We don't know that answer yet.

Maria Losito: If you find out please let me know, though I’m sure that’ll be years down the line, especially if you're doing collab research.

Robin Orozco: That'll be the next paper. You could have me and Obed back and we can talk about it.

Maria Losito: I would love that. What would you say inspires your work as a researcher?

Robin Orozco: I think it’s really trying to understand why people get sick and some people don't. Especially with the pandemic that happened several years back now, but even before that, I think we can look into our communities and see that maybe it's seasonal flu, or maybe it is with different people getting cancer. You notice some people get sick and the next day they seem totally fine; they're running a marathon.

I’m like, ‘how do you do that?’ And then you look at someone who is exposed to the same thing, the same cold virus, and they're bedridden for weeks or sometimes they're hospitalized. So, this array of disease severity really intrigues me, and I want to know why. Why is that happening and what is going on there?

There's a lot of things that feed into that. It's not a one answer but one is how our immune system is functioning and another is that the genetic components that exist in all cells -getting back to this allelic diversity in these mutations.

That’s really what intrigued me, is how do these mutations and genes that change how our immune system function? How does that functional change impact disease severity?  Does that give us insight into, you could argue, the more philosophical, why are some people sick and some people healthy? That gives us insight into understanding how our immune system is functioning and how it is overcoming or adapting evolutionarily as it continues to be exposed to new pathogens.

Maria Losito: Yeah, it's always fascinating to think about how some people get sicker than others. My mother, [when I was] growing up, worked in elementary school as a paraeducator and so she'd always bring back kid crud, just whatever kid sickness was going around. And so for the longest time, I would never really get sick because I just get these little micro colds because of just this constant influx of germs, and then I remember a few years after I'd moved out, and started living on my own and with roommates, that ingrained immunity disappeared and colds started hitting slightly harder than I was used to. So, yeah, it's interesting to see how that shift is and how it impacts things.

Robin Orozco: Yes, you say that and immediately my immunology brain comes on. I'm interested, ‘What was young Maria's immune status when she was young? And was she in a constant state of activation? And okay, so then did that wane and how did that work and what would control that?’ and stuff like that. Not to feel like I'm reducing you to a subject!

Maria Losito: No please, go for it.

Robin Orozco: It's fascinating and I think that's another interesting question. There are people who study that, there are immunologists who are really interested in allergies-that's an immune mediated pathology- and I think most everyone either has or knows someone who has an allergy. Sometimes, you're born with some allergies- I’ve heard many stories of someone who was like, ‘I wasn't allergic to shellfish and went to Canada and had some shrimp and all of a sudden was allergic to shellfish.’

 We have these late onset allergies as well, whether that's due to food allergies or maybe a major type of allergy like pollen. I'm not studying it, but other immunologists are-that as we age our immune status changes. So again, the question becomes why? Why is this happening? Could it be environmental factors? [Which] absolutely plays a role, that includes not only the pollution, or secondhand smoke, or diet that we're experiencing, just a lot of environmental factors, but also our genetics can also potentially impact that as well.

Maria Losito: There’s an interesting aspect to the research that we're really going to be diving into today, would you mind telling us a bit about preprint versus peer reviewed published papers?

Robin Orozco: In the scientific world - I'm going to focus on more biology because that's the larger field that I'm in, Immunology is a subsection of biology- for our papers, we do a bunch of research, we write it all up into a manuscript, and we send it to a journal. When it goes to that journal, there is this long process of the editors looking at it and figuring out, will this paper be appropriate for our journal or not?

If the answer is no, they just send it back immediately and they say, no, we're not taking this. And you go through this process over and over again until a Journal says, yes, we think this is a paper would be appropriate for our journal. From there, they send it out to other experts in the field who review your paper and look at everything fine tooth comb.

If you've ever had one of those tough professors in class, and you're wondering, why are they being so nitpicky about my paper? That's got nothing on the reviewer for a journal article. So, they're looking at how you're representing your data, how you're talking about your data, what are the references you used, did you have the appropriate controls?

They're really looking at the scientific integrity and interest in this article. There are multiple reviewers that happen for every paper, usually 2 to 3. but I've heard of people sometimes having up to seven reviewers. They write up their recommendations, what they think needs to be done to the paper to improve it. Sometimes they put in things that they like as well, if they're feeling generous and happy that day. They send it back to the editor, and then the editor has to decide, are these changes enough? Are these changes actually addressable so that we can give the authors another shot?’ Is it just so bad, we just have to say no or do these changes not matter?

Usually, it's let's give them a shot at making these changes. You do this process 2 to 3 times and if you can imagine, these are not professional paper reviewers, these are your professors, these are professionals in the field. They have jobs other than reviewing papers. It's just one aspect of our job as scientists. It takes them time to review. It takes time for the editors, and it takes time for the lab to address the reviews. There's this very long process to actually get a paper out.

There’s a joke that by the time your paper is published, you don't even want to look at it. You're just so sick of looking at it by that point. Sometimes in the scientific community, we just want to get a paper out. We just want to say, listen, we're going through the process. We're going through the peer review process. We're going through all these changes. We're doing our due diligence, but we want you to know we did something, we did this! That's where preprint servers come in.

There's a lot of controversy about the benefits of preprint servers, or if they should be allowed. But for my lab, the paper that we're going to dive into is the first paper to explore a lot of unique things, and we just want to put this out so that people know we're working on this and that people can use this as a resource, and we can also share with the world, ‘Hey, we're doing something!’, with the understanding that what we're posting has not gone through the peer review process yet.

There's this server called BioRxiv, which is a preprint server. A lot of the time if you start looking at papers, if you look up this paper that we're going to talk about, it'll show up on BioRxiv and it's important to know that, again, that paper has not gone through the peer review process.

That it’s just a paper. You can put basically anything you want up on BioRxiv. So, if you're going to read a BioRxiv paper you really have to have your critical thinking hat on. To make sure to be thinking about [the fact] this paper has not passed the muster of peer review yet, that's where our paper is now.

It's up on BioRxiv as we're going through this review process, in what we call a preprint server. We're in our second or third-ish round of reviews right now. Our fingers are crossed that it is formally accepted soon. We see a light at the end of the tunnel and then once it is accepted, we'll update the preprint server to say, here's the published version that's been accepted by this journal.

Maria Losito: Thank you for telling us and I'm so sorry that you're still in that endless wash cycle of editing and reviewing, that's never a good time.

Robin Orozco: It’s definitely frustrating at times, but also, I try to take a step back and think about how it works. This is how we know that the papers were reading that are in reputable journals have really gone through the process, right? If we didn't, if it wasn't maybe a little bit frustrating, that might raise a red flag in my head, like, ‘Why aren't they criticizing that? My lab is pretty good, but are we that good? We’re not perfect, right?’ So, yeah, it's frustrating, but in the end it does put out a better product. A product that we know has really passed all these tests that we can be really proud of.

Maria Losito: Yeah, that makes sense, I'd prefer to have a well-tested washer than one that I got off the street.

Robin Orozco: Exactly, exactly.

Maria Losito:  Let’s dive into your preprint paper, which is titled“An Autoimmunity-associated allele of PTPN22 enhances innate antiviral immunity to protect against acute coronavirus infection”, what can you tell us about this research?

Robin Orozco: As I mentioned before, the gene we're studying is called PTPN22, and we're studying this allelic variant that again is present in about 5 to 15% of the North American population, and if humans have this, you're more likely to get autoimmunity. So that’s the first half of that title, an autoimmune associated allele of PTPN22.

Prior to this work, we were able to show that using a mouse model - I'm not going around infecting people- We were able to show that if mice had this mutation, that if we gave them a chronic virus infection, they were able to clear that chronic virus infection and do much better than mice that are that don't have this mutation.

This was associated with the change in the immune response, and we mostly focused on an immune cell called the CD4 T cell. We also showed that when giving cancer to mice that have the mutation, that in certain types of cancer models those mice were more resistant to tumor growth. We again looked at the immune response and really focused on an immune cell called the CB8 T-cell.

In both these situations, the chronic virus and the cancer, these are chronic long-term diseases that our animal models, in the wild-type mice they don't fully recover from. We wanted to know in a very different type of infection setting, would we still see a benefit of this allele?

That's what led us to the coronavirus infection. The specific coronavirus we use is called murine hepatitis virus strain A59 or MHV-A59. It infects livers and in a normal wild-type mouse, the mouse will get sick for about a week and about 50% of the mice succumb to the infection, and about 50% go on totally fine and they clear the virus.

It’s similar to what we might have seen in a pandemic situation. It’s important as this is very fast. It's a weak chronic virus infection that can last 100 days in some mice. So, it's a very fast, quick acting infection and again, if mice survive the symptoms, they're good for rest of their lives.

We were like, “Okay, so this is a very different set of immune cells working together to clear this infection. Does our mutation have a benefit?”, and the long story short, what we really show in the first figure is yes, if mice have this mutation, we have a 100% survival in the mice when they have this coronavirus infection compared to wild-type mice.

Then as it's our favorite thing to do, we started to look into what is the immune reason behind this protection. It was through doing these assays that it led us to an innate immune cell called the Natural killer cell.  Natural killer cells are not new, people have known about them for a long time, but prior to our paper, no one had really looked at what PTPN22 does in Natural killer cells, it largely has been ignored.

 There was only one paper on it, and there wasn't a whole lot of work associated with that paper. For us, this was really exciting because by studying this gene and its allele in this new context for us, it led us to studying this cell type, but the gene had not been looked at, and there was a scientific rationale for it now.

This paper goes through the importance of the Natural killer cell in this infection, and we were able to show that when Natural killer cells have this mutation, they gain an ability- kind of like a superhero, right? Bitten by the radioactive spider- they now gain these abilities to help fight off the infection or in the mice that don't have this mutation, the Natural killer cells actually don't have that big of a role.

Maria Losito: Okay, wow, that's so much, and I’m just sort of digesting it all, but to be able to go down these two different paths of studying cells and get results, that's really exciting that it didn't end up being just sort of a path to nowhere.

Robin Orozco: Yeah, it was exciting. When I started my lab at KU in July of 2022, I started a collaboration with Tony Fehr, who's recently on the podcast. Tony and I’s research labs are next to each other, our lab are friends, we joke we need to knock the wall down between our labs, because then they wouldn’t have to go in the hallway to visit each other. They can just go through the doorway. 

He was really generous, Tony is a coronavirus expert, and they had this coronavirus, and he was like, ‘I have this acute model, is that something you want to test? Should we just see if it works?’ 

It was actually his senior graduate student, Catherine Kerr, who ran the first studies of this, and it was the first data that came out of my lab. As a new PI, I was just out of my postdoc and I was like, ‘What's my lab? Oh, gosh, what are we going to do? I hope there's something here.’

We had this protective phenotype and graduate student, Alec Bevis, joined the lab my first year. He really took on this project, and it was he who started doing experiments to try to explain why we had this phenotype.

It's very much a detective type thing. So, Alex had to read and I read a lot of papers trying to figure out, what do we know about this infection? What do people know? What do we know about PTPN22?

Natural killer cells were not on our mind when we started this. We did an experiment where we used mice that lack adaptive immune cells, so, T-cells and B-cells, and we saw that they were still partially protected. We weren't expecting that to be honest, I thought there was not going to be protection, or at least partial protection. I thought it was going to look the same .That was  a fun result and that really then steered us to looking at the innate immune response and we eventually got to the Natural killer cells from there.

Maria Losito: Ever since I started at KU and started doing these interviews with faculty, way at the start when it was just ‘Get to Know Your Faculty’ type interviews, to now on the podcast, I've always been surprised by how collaborative the science world is. I was an illustration major, and I never expected to join this side of the world. I never expected that collaboration from scientists. You get this idea of the movie scientists, where there're off in their own dramatic lab doing their own thing. No one else is really there, and everyone's like, ‘no, stop that’. [Where in reality, it’s’] yes, can we help’? It's fascinating and just really exciting to hear that there is so much collaboration and it's an additive process and not a subtractive one.

Robin Orozco:

Yeah, I've been in science since I was a sophomore in undergrad and throughout my training, it's always been very clear that science is a team sport. It has to be a team sport, especially now with the amount of different technology we have. And all the interdisciplinary research that exists and should exist. I wish I could know everything, but I don't know everything, and so I need and everyone needs supportive team members to that have different skills to really help. 

I know this is maybe a lame analogy, but I really love watching sports. I've recently gotten into college basketball, which is probably fitting being here at KU, and I've been able to go to a few of the games and in my limited knowledge of how basketball works, it's still very obvious to me that different players have different roles and strengths, but they come together in a team that becomes a championship level team. That's also true of science. 

Throughout my training, I've seen this, I've been encouraged to continue to do this. As a people person and an extrovert, it also makes my job much more satisfying to be able to be interacting with a lot of really brilliant people who are so passionate about what they do and really care about what they do, and they care about their teams to be in that environment and to be solving  these unknown questions.

Maria Losito: Well, that was a huge digression, so I apologize, but that's what talking to me is like. 

Robin Orozco: Same, I’m glad I'm not alone.

Maria Losito: So back to your paper, we talked about the alleles, we talked about how that was impacting antiviral immunity across different viruses. Why is it important for the everyday person?

Robin Orozco: So as we think way back to the beginning of this podcast, I talked about understanding the fundamentals of the immune response. When I grew up, my dad was always in construction work, He worked in a lumber yard, did all these different things, very blue-collar work. My grandpa was a contractor and built houses and so growing up, a lot of my conversations that were around the dinner table were about how things were built and how things are put together and stabilized. There was a lot of conversation about, ‘oh, yeah, all these new builds, their foundation is bad or it's shoddy craftsmanship.’They’re ignoring the fundamentals of building a home and that's going to make for a weaker home. You can't go with shortcuts. But in order to know what it is to make a strong foundation and build a strong home; you have to know and understand those parts.

If you want to break the traditional rules, or you don't have a certain supply, [ you need to understand why they use] that particular supply, why that particular type of wood, whether, it's oak versus walnut versus cherry, or a two by four versus a two by six, why that is used versus something else, then you can find the appropriate alternative. Understanding fundamental biology and fundamental immunology is the same.

If we don't understand how our cells work and work together, and we don't understand what happens when we have different mutations or different context, if we ever hope to continue to exploit the immune system for therapy or even therapies that aren't aimed at exploiting the immune system, but just targeted anyway, because we have immune systems and we see something going wrong, we might not be able to figure out why without understanding the basics of it first.

I really think, fundamental biology, while the translation of that of impacting maybe human health or, improving human lifestyle seems far removed, it's really important. I don't think anyone would like to live in a house that someone built if the builder didn't understand the materials they were using. I think that can be true of when we think about translational and clinical applications of biology and all science for that matter.

Maria Losito: We talked about using mouse mirroring models, what other aspects did you utilize in the lab to get your results?

Robin Orozco: I would say mostly use the mouse model and we do that for a few reasons. One, in our mouse models, we can make sure that we limit the variables. We just want this mutation that's changing in our mice. Once we go to human cell lines there's a lot more variables that can change. Those studies are appropriate at times, but for this particular question they weren't as appropriate. 

When we have this mouse model we then use as much of the mouse and the information from the mouse as we can. After the infection or certain parts of the infection we look at the immune response going on in the mouse.

We're able to take the livers from these mice and look at what the immune system was actually doing there. We use a method called flow cytometry to do that. We can take the cells, put them in a single cell suspension, and stain them with antibodies.

Actually, people often know about antibodies because that's what your vaccines help create. We have antibodies that are specific to different proteins, and they have a fluorescent tag on them. We can put them in this machine that uses lasers and we can start identifying what cells are there. We can also use flow cytometry to help us say what the function of those cells are. We do a lot of flow cytometry in the paper to help us identify cell types and specifically immune cell types, and what they're doing in our different animals.

We also use histology. We sent the livers off to a pathologist at Oklahoma State University, Sunil More, who's on the paper, and he was able to do the histology on it and stain for liver damage and see what was going on there. We also use cell culture in the lab as well. We can use other types of antibodies to actually deplete cell types in the mouse. We were able to get rid of the Natural killer cells in our animals to see if the Natural killer cells were actually important in our infection or not.

It's a pretty big paper, it's really thorough. I think Alec did a really wonderful job, being really rigorous and thorough in his approach.

Maria Losito:  During your study, what kind of findings did you have? What do those findings mean for further research?

Robin Orozco: In this study, I think the two main takeaways are that this mutation does protect during an acute virus infection that impacts the liver. What we didn't talk about is that this mutation doesn't cause a loss of the protein, the protein is still there; it just has altered function.

We also had animals in the study that lacked PTPN22 expression. They didn't make the gene or the protein product from this gene at all. The mutation of the gene and the knockout of the gene are not always the same. They don't act the same and often in research if we see a mutation, people will often liken it to, ‘oh, if I just knock out the gene it’s the same as having the mutation,’ and that's not the situation.

I think that's an important thing for us as we think forward in our research, to really consider that move forward, that the knockout is not necessarily the same as the mutation. Sometimes it is, sometimes it's not. We're trying to figure out when it is and when it's not, what the rules are.

The other thing is we looked at a different type of virus infection, very different than what we've looked at before, and in a different organ than what we've looked at before. Where before we were mostly looking at the spleen this gave us new insight into what was going on. We started looking at the Natural killer cell. There was a different pathology. It raises questions of context dependent effects. This was an acute virus in the liver. When we think of the Covid pandemic we actually think of respiratory infections, so would this be the same in the lungs? We don't know. There are lung resident immune cells and maybe they have a specific effect.

We have a different project in the lab right now looking at the immune cells in adipose tissue and we're seeing a completely different cell type called the natural killer T cell, that seems to have an effect. This research is starting to highlight or maybe continue to highlight, we really must consider the context and what we're looking at. Whether that's the type of infection, the organ we're looking at, the time point we're looking at, and that this gene has a different effect on the cells depending on that. Figuring out those details will probably be a lifelong career for me and that's important because again, if let's say we ever wanted to exploit these protective effects of PTPN22, if you have a patient come into the hospital knowing that they have a lung infection versus a liver, maybe, an encephalitic, it may change how you think about exploiting this particular molecule. Also, the time point in which they are in their infection, is it a chronic situation? Is it an acute Infection? All of those variables would come into best treat that patient and give them the best shot at overcoming the infection.

Maria Losito: You mentioned that previously you were working on the spleen and then ended up shifting towards the liver. Was that because the virus that we're currently seeing in this paper was a liver based virus and then it wasn't really appearing in the spleen?

Robin Orozco: When we looked at the chronic infection, it mostly affects the spleen, and we know the spleen is the main site of infection from other work and an important aspect of where the immune system is at getting activated. We are focused on the spleen in the chronic infection, we could have looked at other organs as well- it does also go to the lungs, but we didn't look at that. For this virus, MHV, the coronavirus, we also looked at the spleen as well because it is a main immune organ, but the liver is the main site of infection. So MHV does infect the spleen just at a much lower level.

It’s really that main site of infection and so we wanted to know where the infection is mostly happening and where we have that most antigen load. What is the immune system doing there, right? Location matters. We really focused on the liver but in the supplemental figures, we also look in the spleen to see what's going on. In the spleen we see the same stuff as we see in the liver just to a lesser degree, which makes sense.

Maria Losito: Is there anything that we didn't talk about that you think we should?

Robin Orozco: Yeah, I think the philosophical side of this paper's journey was when we set out to do this paper and do these studies, I certainly had ideas about what I thought was going to happen and what the effect was going to be and what immune cells were going to be key players in that. And I was wrong and that's okay.

As scientists, I think it's important to remember, and especially as people training to be scientists, when we come to work, it's not about if we're right or wrong, we  have to check our egos at the door and our experiments are not to prove ourselves right. The data is the data, and we have to follow that.

It's our job as scientists to take what the experiments tell us and to think critically about that and think about what that means, and then do our next step forward. I think this paper was a great lesson in that and at the end of the day, I think this paper uncovered truth and fact, which is important.

But setting out, this paper also showed me I was wrong in my assumptions about what I thought was going wrong or what was going to happen. I think that's  an important aspect to always remember as we go through the scientific process and as we think about entering in and conducting research.

Maria Losito:  Yeah, honestly, I feel like that's good life advice for science and beyond.

Robin Orozco: Yeah, always be ready to accept that what you think isn’t right. Always be ready to be wrong.

Maria Losito: Always be ready to be wrong, I mean, sometimes it's just your opening doors to learn.

Robin Orozco: You’ve got to keep what they call the growth mindset alive. Always be ready to grow in your previously held assumptions or “facts” of what you know and being able to think critically through that as well. There's a day in age of a lot of misinformation and a lot of stuff that's thrown at us, that is or is not substantiated and we’ve got to figure it out.

Maria Losito:  Yeah, I spent a lot of my day on social media, making social media posts and, yeah, just the amount of misinformation that is out there that as you're scrolling quickly, that you see and you don't really think about, and sometimes you need to take a few extra seconds, think about what you just saw, and then move on.

Robin Orozco: Yeah.

Maria Losito: Well, thank you so much, Dr. Orozco, I really appreciate you coming by today.

Robin Orozco: Thanks for having me.

Maria Losito: Thank you for listening to Interview with a Biologist. You can check out the show notes for more information about Doctor Orozco's work, as well as a link to the research paper discussed in this episode. A full transcript of this episode is available at biology.ku.edu.