0:00  
Jim: Welcome back to the Plantopia podcast, the plant health podcast produced by the American Phytopathological Society. I'm your host, Jim Bradeen, professor of plant pathology and Associate Vice President for strategy at Colorado State University. And today I'm delighted to welcome Juliana Gonzalez Tobon. Juliana is a PhD plant pathology student at Cornell University, where she studies the role of small non-coding RNAs in regulating interactions between plant pathogens and their hosts. Juliana first came to love plant pathology as an undergraduate student at Universidad de luz de Los Angeles in Bogota, Colombia. And Juliana has a very impressive publication and presentation record for an early career scientists. Today we're going to talk a little bit about her current research. And we're also going to explore her motivation behind efforts to use social media to fight COVID misinformation and effort that combines her unique research history and interests. Juliana, thank you so much for joining us on Plantopia.

1:14  
Juliana: Jim, thank you so much for that introduction, super excited to be here. I've listened to all the episodes that have been out. I'm just so happy and honored to be here.

1:27  
Jim: That's fantastic. Thank you so much. Again, I really want to know a little bit about you as a person, how you you got into plant pathology, I understand as an undergrad student, you you started your studies thinking you wanted to work in the area of human genetics.

1:46  
Juliana: Yeah.

1:47  
Jim: How did you ended up in plant path?

1:49  
Juliana: Well, when I when I was, you know, deciding what to do as a career and just picking an undergrad, you know, program, I was very set on wanting to do something that will lead me to work in human genetics and human cancer research. Mostly, I have like a very strong personal motivation to do that. And in Borneo, Cialis on this, which is my alma mater back in Colombia, they have two programs. One is biology and the other is microbiology. And honestly, when I was speaking, you know, what to do, I had no idea with microbiology was. So I was like, well, let's go with biology, which is what I understand, and what I know, could lead me to what I want to do. During you know, the process, it was a four year program. And about, after two years, I realized that yeah, I liked that. But I was much more of like a lab person than I'm, you know, outgoing, 100 person field person. And that's a little bit where the biology career was focused there. So I decided to do both, they gave you the option of Do you know, mix sort of mix and match programs. So I did both of them. And that's the point where I started to try, you know, join labs to gain experience in what I wanted to do right in molecular biology in research. And I joined joined a human genetics lab. And I was very close, honestly, to just do my dissertation there and just continue there. But situations in that lab that led to me being in a moment where there was no really like an advisor that was available to guide me in which I specifically wanted back then, I didn't feel very supportive there. And I did remember that I had just taking like a class that's called a sort of fungal biology or just fungi in general, with Silvia Restrepo you who you might know for MPs, and I want to talk to her and I said, I'm not sure this is the life for me, I'm not sure I'm gonna have like the chances of research. But I do know, I like pathogens. I do know I like Microbiology and Molecular Biology. And I have just seen also a class called epigenetics. And I was like, This is amazing. I want to do everything in this in my life. And she was like, Well, I love everything that you're saying, and you're super welcome in my love, but I don't work with humans. I work with plants. And I was like, what and that was the moment I started to understand that you know, we have human TC says we have human research. Then we have plenty thesis and plant science research and the importance of that. And it all sort of match at you know, those moments in science where everything sort of comes into place in your favor. I was also starting to take a class basically called plant pathology, and just everything came together in my mind and I was like, This is it. This is what I want to do. She opened the doors to her left to meet and I did to undergrad thesis actually right there because they want to do one for the biology program and one for the microbiology program, and then I just ended up with so many questions that I stayed. And I did my masters. They're all in plant pathology. So yeah, that was the beginning of it.

5:15  
Jim: That's amazing it you know, the importance of good mentors and have those firsthand experiences really, really critical for so many of us in this field. You mentioned your masters, and I recently saw a preprint on the Bio Archive Server that I think came from your master's research. The title of that is "Evaluation of Small Non-Coding RNAs As a Possible Epigenetic Mechanism, Mediating the Transformation from Biotrophy to Necrotrophy In the Life Cycle of Phytophthora infestans". So there's a lot of great information just in the title. I think in plant pathology, many of us probably know it, photographer infestans is, but for our broader listenership, tell us a little bit about photographer infestans and why we care about this thing.

6:14  
Juliana: Yeah. And that's perfect to actually continue with the story. Because when I ended up in Sylvia's lab, she worked with different things. But her main focus at that moment was Phytophthora infestans, which, you know, the common name would be late blight. And it's a very important disease, both in Colombia where I'm from, and in the world, basically, I don't know if you know, a more broader listener has heard about the big famine that happened in in Ireland's like 1800s, that basically wiped off 30% of their population, it was also one of the main drivers, for a lot of people, they're migrating to the United States and just looking for, you know, starting life in a different place. And that was because these pathogen is so destructive, so extremely destructive, that it basically was wiping off their potato crops, which was one of their main, you know, food resources that they had there. And also just economy resource, because they were also growing and selling that. And this, you know, it's interesting to think that this pathogen has been around for so long. And it's a steal a very big problem. And it's a steal something that worries plant pathologist a lot. So when I heard about all this story in fight after investments, and I had the opportunity to work in this lab, that it was really trying to understand it better in Colombia, to use information from the you know, United States lineages that we have here and then understand what we have down during Colombia. I was like, this is very exciting. So what I did, both, I can make sort of undergrad and masters because it ended up being you know, all together in almost three different articles. If I can divide it into parts, one is the one that you're mentioning, which is tried to really understand the molecular interactions that these pathogen has, when it is infecting or when it is, you know, just thriving in the plant. And in that sense, that's still a work in progress that when you read, that's why it's still a preprint. Well, we also already published this one, we wanted to see if small RNAs, which are something that has gained more attention in more recent years. But back then this was like 2015-2016, maybe it didn't really was not really much studied in this pathogen. Yet. There were papers, of course, but nothing from Colombia, nothing, you know, done there. And I wanted to understand how it could impact how this pathogen attacks the plant. And that's where the funny words you're reading come from, by atrophy and nichrome atrophy to go ahead.

6:27  
Jim: Let me ask a quick question, though. What is a small non-coding RNA?

9:12  
Juliana: Great question. Well, I think most people are familiar now, especially after the pandemic, with just the word RNA, right? And how it's these molecule that's very important in every single living being. And we have different types of RNA. This one, the small non coding one, are very small. And when I'm talking smaller, like, you know, 20 v spurs, especially in fight after they were really, really small, that are really interesting, because their sequence just, you know, normal RNA sequence matches places in the genome. And the reason why they match different places in the genome genome is because they will guide a whole protein complex to whichever location they match to. And then that protein complex will help degrade, for example, an RNA transcript before it becomes protein or we can pay for it produces a protein. So these, we all know, the normal, you know, molecular biology dogma where we go from DNA, our genes, which are basically our instructions, right in ourselves or the pathogen cells, then we go to RNA, which is these transition from the gene to the protein sort of I explain it in more broader terms is like an instruction, as if you're taking notes from a book before you actually go on to something with that. And then the end product or the result, which will be the proteins. So the small RNAs are, you know, an additional thing that comes into play in all these normal process where they can help us regulate which of these trans transcripts or normal RNAs as we mostly know them from whether they become a generate protein or not. And that is one of the reasons why it this is part of what we know, as epigenetics, which I mean, maybe we can get into detail later. But in general terms, we have genetics, right, where you have your genes and your genes say exactly what they are meant to say. But then you have epigenetics, which are these other processes that happen in the cells and decide or regulate whether those genes are becoming protein? When are they coming protein? And, you know, in which parts, in our case, our body, in the pathogens case? Well, it's different structures.

11:42  
Jim: Great explanation, I appreciate that clarity. So how is the top two infestans using these non-coding RNAs?

11:50  
Juliana: Well, that's what we are trying to figure out. But I can tell you two things for these preprint that we're still working on, fight after, does something that some pathogens do, but not all, which is it starts living in the plant, let's say a potato plant, and it started starts feeding on it, it eats the, you know, living tissue that leaves the tubers, even the stems, in some cases. And then at some point during its lifecycle, it just makes a switch. And it starts being really aggressive, killing all of it. So not keeping it alive, just really making the tissue become necrotic. And, you know, death. And that's what we call micratrophy. So that's why this pathogen is an Emmy biotropic pathogen, because it goes from biotrophy to necrotrophy. Other pathogens are always necrotic, like the moment they get there, they just kill everything. Others, I always biotrophy. So like they get there on the Muntean the plant alive to fit from that. And what we think we're trying to show with this paper, that I hope will be finished soon, is that maybe these small non coding RNAs are helping it turn on and off certain genes, depending on the moment of the cycle where it needs to be.

13:16  
Jim: So it really needs to regulate its own genes, right? In certain certain proteins, at certain times in that infection process. 

13:27  
Juliana: Exactly. And that's what you know, usually happens with pathogens, but I felt when I was starting in plant pathology, that I wanted to understand that better, because pathogens not don't work the same at every single moment, they have to adjust and they have to adapt to the environment where they're at the you know, the amount of food they find the type of plant, they're facing, the variety that they're facing. So there's so many different things that yes, we have explanations for some of them that are very clear and like are very genetic based. But there were others that that seemed to me, at least with Phytophthora didn't have such a clear genetic explanation. They might have just that regulatory explanation behind them.

14:14  
Jim: It really strikes me you mentioned that the Irish potato famine or the European potato famine of the 1840s. It really strikes me that we have we as a research community have done a lot of work on Fatah through infestans and the potato Lake flight path system. But we're, you know, 180 years almost out from the Irish potato famine, and there's still so much to learn about that about the pathogen and the host in their interactions. Yeah, really exciting work.

14:51  
Juliana: Yeah, and that actually gives me a little bit of moment to tell you very quickly and you can then decide if this makes sense about out another project we had during my master, which is actually already published that this one you guys can read more easily. And it all stemmed from a mistake, if you want to call it like that, that happened here at Cornell in Dr. Bill Fry's lab years ago, like seven years ago. And it was because as we have been saying, since by tougher is so aggressive, and so difficult to manage, one of the things that you know, the community has done in the plan scientists have done during these years to control it, is just use fungicides and just chemical compounds to control it. And that's, you know, what mostly people use in the field and growers use in their farms. So this lab, Dr. Bill Fry's lab, who has done amazing work in Phytophthora. For so many years, they were testing different fungicides and specifically one that's called My Fennec some very commonly used here in the US at different concentrations of it to see you know, which ones of the lineages that they had in the lab, mostly from New York states, were susceptible to the fungicide or resistant to it and in what concentrations. And, you know, imagine they were testing in a plate, which zero fungicides so the pathogen can leave happily there. And then a meat concentration where, you know, it was enough to control its growth, but it was not enough to fully wipe it off. And then another one with a lot more fungicide to the level where it's just lethal to it. And they were just making your own routine very transfers from one to the other. And someone just messed it up in the sense that, instead of making the transfer from the original one, without fungicide, they made a transfer from the mid concentration. So the one that regulated it, but not killed that. And then when they passed it to, you know, the same set of concentrations, again, the pathogen was able to grow in all of them, even the lethal one, as if there was no fungicide there. And this is one of those things in science that sort of comes by serendipity. And you're like, Oh, I thought this was a mistake. But maybe No, maybe it's something. Let's make an experiment, right, let's plan an experiment to test that. And when they tested it, I turned out that it repeated, which is what we're looking for, right a scientist to see if things replicate and happen again. And it happened in different lineages. It happened in different times that they repeated it. That ended up generating a paper in I think it's phytopathology 2015. And in that paper, one of the authors is Giovanna Aeneas, who was in that moment, PhD student in Dr. Fries lab. But then she went back to Columbia, because she was originally from Columbia, and then ended up being my teacher of them pathology. And when she told us about this, I was like, That is amazing. She also said, you know, after they acquired, they were calling it acquired resistance. If you put it back in media, without the fungicide it progressively loses that resistance. So it's not like the common fungicide resistance that we already know of where you gain it. And like that's it, the population is very resistant, nothing to

18:27  
Jim: So that suggested it wasn't a genetic change. 

18:29  
Juliana: Exactly. That's just that it was a genetic change to an epigenetic one. And that was one of the main drivers that it was like, I need to study this. And then the other paper I was mentioning, which was actually published last year, in plant disease, we made all these set of molecular biology techniques, including small RNA testing, as you were mentioning earlier, to try and understand what are the things that are changing in the pathogen, when it gets resistant, and then when it goes back to sort of losing that. And honestly, that's one of the papers that I'm most proud of just because it was so much work so many years put in that. But it's a good way. And I think it's a very beautiful way to sort of show how pathogens are not static things they change. And part of the challenge for us as scientists, and you know, plant pathologist is understand how that change goes, how we can play with that to our advantage.

19:35  
Jim: I really love that. And it makes me think of the the many, many times I've talked to different plant pathologist working in different path systems where, you know, essentially they describe the plant pathogen growing in culture, and it getting kind of lazy, less, less well adapted to the host. And I think what You're describing as a really good case of that. And really interesting that that you've been able to pinpoint an epigenetic origin for this. I think it explains a lot in our science. And I wanted to mention that on the plane topia podcast dot work, which is the official landing page for this will include links to all of the papers that we've referenced today. So it sounds like you had a really, incredibly productive and exciting master's program. And now you're at Cornell as a PhD student. I guess first of all, how did you get to Cornell? Why Cornell and what are you doing today?

20:38  
Juliana: Yes. So you know, I've mentioned my two mentors from when you already understand this your best friend Joanna? And yes, they were both 100%. For Cornell, Joanna was, as I said, a PhD student here. And then Silvia did her postdoc here. So when I was finishing my master's, I sort of said, you know, I want to stay in academia, I feel like I want to keep researching. But I'm a little bit lost as to what to do now. And they both say, well just go and do a PhD. And I said, I have no money to do a PhD. And they say, usually nobody does. That's why we find for, you know, funding. That's why we look for places that have programs for funding. And they said, you know, Cornell is an amazing place. So in 2017, which was between the end of my undergrad and the beginning of my master, we had already talked about, you know, future in research, I had the opportunity to come to Cornell during the summer, basically, it was from June to August, and just be an intern in one of the plant pathology labs. That summer, I was part of Dr. Keith Perry's lab. And it was a little bit different because they work with viruses, but also, small RNAs, they in that case, they use small RNAs to understand which viruses they were finding in vines population here in the Finger Lakes, which super important in this region for wine production. And so that was an amazing experience, not only in research, you know, sense. And I learned a lot from them. But also just in going outside of my country, seeing how science was being done outside in the US in a gigantic institution as Cornell and figuring if, you know, it felt like a place for me as like long term. And it did, I came back home feeling that I didn't want to do long term research here. And I guess I just tried to come back as much as I could. The following summer, which was one day when I was 100%, into my master's, we realized that it was easier for me to come here and do some of my experiments in Dr. Fries lab, instead of like importing everything we needed and all the reagents and everything to Colombia, which is one of the challenges of doing research in smaller countries. So I did, I came here, I just confirmed that this was the place for me. And as soon as they came back, I applied to start my PhD in then next fall, I was a little bit reckless in the sense that I only applied to Cornell. I then realized when I was invited as a, you know, recruiting students, that all the other people that were here with me how to apply to 10s of universities. And they were like, which, you know, which are your choices, and that was like, only applied to Cornell? Like,

23:44  
Jim: I like that confidence.

23:45  
Juliana: I don't know, I think it was a mixture of confidence, but also just like, I didn't know, I was not aware that you had to have. I was sort of like, if Cornell says no, then I'll just stay here for more, you know, for longer and look for something else to do here. But fortunately, that they said yes. And I came and started my PhD in 2019 Right before the pandemic hit.

24:16  
Jim: That's great. And Cornell certainly is a great institution. What's it been like though, as a graduate student in this pandemic period?

24:25  
Juliana: It has been challenging, I can say I started in June so that meant that I had the summer and the fall in sort of like a normal campus and a normal situation. I you know, I went to classes I just normally what you do as a first year PhD student is like go to classes and start thinking about your research, do with small projects in the lab and just get it, you know, accustomed to it and to the people. But then as soon as the spring semester started, things started to look strange and you know, news kept coming of these viruses It was around. And then mid March, there was just one day that Cornell sent an email and said, you know, we're gonna bring the spring break closer, and we're gonna send the undergrads home, if you're a grad student, of course, you can stay, but you cannot work in the lab until further notice. That's it. And I guess, you know, as probably everybody that is listening to this, you know, felt very scared. In my case, also, I think I have the additional challenge of being an international student. And I felt like I just moved here, I didn't even enjoy a full year. And I was not sure if we were going to be able to stay or what it was going to happen. And I say we because my husband moved here with me, like I moved my whole life here. It's not that I just came myself. But I think my advisor, which is Dr. Amelia and Melanie Phillips, right here at Cornell, she was super flexible, she was super understanding. And she said, Well, we're just gonna make the best of this situation, we were not able to go back to the lab for about two or three months. So during that time, I to read a lot of bioinformatics, I guess I benefited from the sense that I was just starting, and I was in a stage where I was planning most of what I was going to do. So you know, having time to sit down, look at the data, go into the genomes, download things, and start just thinking of what I wanted to do in the lab. But sort of doing like a pre approach from my computer. That was very helpful. So when I came back into the lab during the summer, I felt I was more productive, just because I had so much time to think that through. But after that it has just been a challenge of like, you know, moments when we were allowed to go in the lab, we had restrictions of how many people would be there and at what times. So you had planned your experiments really well, so that they fit in the time that you were able to go into the lab and not lose any time. And now that that's much more relaxed, I feel I have not stepped back from that. So when I go to a lab and like super concentrated and and I do all these things, and then I realized, well, you know, I can take it more slowly, I don't need to get out of here in like two hours. So yeah, but I think the biggest challenge more like aside from the research was just not having an in person community around when you're such a young student. Also, my cohort was very small. So we didn't really have other people to rely on. I mean, you could talk to people on Zoom, but it's different. And it's just the difference of Ben going back and seeing these younger cohorts being able to meet in person and like do take all their classes in person. I think it was difficult, but I don't know, I just think we made the best of it.

27:57  
Jim: That story is certainly rings true to me as well. You're describing that sort of the social aspect of science. And, you know, just despite how science is often portrayed in popular press or movies, they're really critical social communal aspects of science, learning from each other, support each other, you know, getting getting to know each other, that's really very critical. And it's certainly something that has been a challenge, particularly during the lockdown face of this pandemic. I'm glad you've come through that period. Well, and I hope that for your sake, and as well as all of ours, that the worst of that is behind us. 

28:43  
Juliana: Yeah. 

28:43  
Jim: Could you could you tell us a little bit about what your PhD research is at this point?

28:49  
Juliana: Yeah. So you know, I came to Cornell with these experience in all my seats. Because I have worked with Phytophthora so much. The scenario here at Cornell was a little bit changing in that moment, there was no lab that was working exactly what I've done before. And that was actually really great. Because I just wanted to use all that experience in molecular biology and maybe apply it in something different. I chose Dr. Melanie fieldtrips lab. She works with bacteria in general that affect plants. She had a very strong focus on Pseudomonas syringae that as you may know, what is one of our model back to Yeah, for, you know, plan the fees, and that has been researched so much by so many people. But then more recently, she has included in her program, another bacterium that's called de cada 20. It was formerly known as Erwinia Kristin Tammy and I mentioned that because I know a lot of you know, season plant pathologies are like Dickeya, like they recognize the old name of course,

29:55  
Jim: is a soft rot pathogen.

29:57  
Juliana: pathogen. Yes. It is very closely related to pectobacterium, which you might have also heard of. And, and yeah, its name was recently changed 2005 It became important, I guess, more important in the US and the eastern time pathology industry and research area is starting in 2018 2019. Because there was an outbreak in basically, that affected basically all the states that produce potatoes. And people were like, What is this? Where is this pathogen coming from is effective bacterium? No, it's not. It's different. What is it, and a lot of, you know, research institutions in the East, including Cornell, decided that they needed to, you know, give a hand and start understanding this pathogen as well, which, curiously, has been more studied in Europe, because it has been generating problems in Europe for a longer time, the species that we have here, and they're a little bit different, but just the general genus has been widely recognized in Europe earlier than here. So my PI included dickeya. In her work, that meant that she included potatoes in her work, and that it was very attractive to me in the sense that I could both do you know, molecular biology and epigenetics, but also continue with the crop that I've been working with. And potatoes are also are not only one of the five major crops grown in the world, are exceedingly important in the US. But they are also very important in Colombia. So I felt that it was also a way to maintain things that are going to be relevant from my, you know, for my home country. So. So what I'm doing with dickeya, going back to that is a very molecular based research as well. I am trying to understand how it senses its environment. So as I mentioned, pathogens have to understand what's going on, and then respond to that. And one of the ways they do that, and mostly bacteria is a process called chemotaxis. And it's just basically sensing chemical cues from the environment and responding to it. Those cues can be, you know, plant compounds, defense compounds that the plants are generating when they're being attacked. And then the bacteria responds to that. So I'm understanding how that process works. But then I'm also understanding if there's, again, an epigenetic mechanism behind that, that will help them be quick and reversible. That's the two things that are most important in a pet genetic mechanisms that they are very quick to do quicker than just, you know, gaining a genetic mutation that gets fixed over time. And again, reversible. And we're looking specifically at a group of genes that are called methyl excepting chemo receptors, but we call them MCPS, for short, that are mainly required for that sensing process that I was saying, I'm curiously decat de Danti, which is one of the species that we're working with has so many of them compared to, you know, closely related pathogens. The question starts where, you know, why does it have so many? Why does it need so many? And how is it regulating that many genes that could be doing the same thing? Or are they not? Maybe they're doing different things? So, you know, I still don't have answers, of course, because I have two more years to go here. But we do know that these genes have a very long upstream region. So right before the gene, it's a region that was considered to be empty, like no genes were there. But previous people from my lab realize that that region is actually being transcribed. And you know, it's being expressed in some sense when the bacteria is impacting the plants. And that just made me think and made us think, well, there's something there that is not empty. What is it there? And up until now, we know that these structures that we're seeing they're very much resemble small RNA structures, and we're trying to understand, you know, which small RNAs are there? Are they actually regulating the genes that are right next to them? Or are they doing something different, but we do know there's something there we're trying to get a hold of it. And if we do understand that, then you know potentially can use that. To control how much these bacteria senses its environment. Of course, there's a super long term goal but everything in molecular biologist starts like that. Like you have to look at the little details before you think of the bigger thing where you can apply that.

34:50  
Jim: That is super, super exciting work. And I really look forward to seeing where this research goes. I think it has broad implications for our basic biological understanding of plant microbe interactions, but also disease control as you sort of reference. Yeah, I'm very, very cool work. I want to take a moment though in pivot to a related topic, you're something of a rock star on Instagram. And if you've got a really robust social media presence, you can follow Juliana on Instagram, on Twitter, on YouTube and Tiktok. All under the handle epi plant path that's E-P-I-P-L-A-N-T-P-A-T-H. I want to talk a particularly about your your Instagram account, you got almost 10,000 followers. Your Instagram account is in Spanish, and really is a professional scientific communication account. Tell us about that account, what you're putting out on Instagram and why you're doing it.

36:02  
Juliana: Okay, I'm gonna ask you a question first, do you have a group chat with your family? Like with your extended family?

36:14  
Jim: Not really, I don't. Okay, we text once in a while, but we don't routinely do that. No.

36:21  
Juliana: Uh huh. Well, the reason why I'm asking that question is, because to explain how this Instagram started, I need to make a point regarding how my roots on my Latin American culture are somehow different in some senses to the way maybe, you know, people here in the US relate to their families. And that's because for some reason, we do have very big family group chat. That's a concept that has been hard to explain to my friends here in the US. They're like, the same as you. They're like, what I mean, I test text, my parents, maybe my grandparents that every now and then I don't listen to, you know, hear from them every single day. And you know, maybe people that are listening and are also from Latin American background, or even a Hispanic background can relate in the sense that for some reason, in our culture is very common to have huge family group chats, where things happen every single day, and they share things every single day. And in my family group shot from Colombia, there's almost 50 people there, which is a lot. And they share everything they see they share everything they consider relevant. And you might imagine that when the pandemic started, they just started sharing every single thing they saw in social media, everything they got in their, you know, WhatsApp chats from friends. And, I mean, that was fine. They were just trying to socialize what was happening, right relate to what was happening. But early 2021, when the vaccines started rolling out here in the US, or at least the first people being vaccinated, starting going to the news. I just started having to deal with messages every single day from my family that were 100% misinformation. There were things like, you know, this vaccines are gonna kill us, or what is it that they call RNA? What are they putting on that? What are they getting that into our bodies?

38:34  
Jim: You may correct that, that most of the folks on on that chat most of your extended family are not scientists.

38:41  
Juliana: Exactly. Yes, there are more. Maybe two scientists and the rest are just general audience people, like they do all other things in their life. And they were very scared. And I think that's the the main thing that made me feel uncomfortable with that I was like, for, you know, to me, seeing and reading about these RNA vaccines was like, the realization of everything we've been talking about, you know, doing very much molecular research, and then making it be useful for the world and for humanity. And I was like, so excited about them about understanding how they work, and why were they going to be rolled out in such a massive sense. But then I went to that chat, and I saw how my aunts and you know, uncles were extremely scared of just conceiving the idea of getting vaccinated with that. So I told my husband one night like, I'm gonna do something about it. I might just post something on my Facebook that I know they read and explain what is RNA very simply, why is it being put into vaccines? What is it doing in our body and why is it not a reason to worry? Instead, it's a reason to be very high. Be about it. And my husband said, you know, I think a video makes more sense, a video gets more people's attention. And I just grabbed my phone, like literally just grabbed it sit down, talked for like eight minutes in Spanish. And it was directly talking to my family. I sort of presented myself at the beginning, like introduce myself, just because I thought, oh, maybe they send it to their friends. So just so they know that I'm not like some crazy person trying to explain RNA. And I finished that, I send it to them in this group chat. And then I thought, well, it wouldn't hurt to just post that in my social media, which at that moment, I had, like 50 friends on Instagram, like just my friends, but I thought maybe they're having the same problem with their own families. And maybe it works for them to share this, I have to clarify that in that moment, there was no information like, you know, accessible about the vaccines in Spanish, there was already things in English, and usually the CDC makes 100 I really good job, putting out in their webpage, explanations that are very simple. But in Spanish, we didn't have any anything like that. And I just did that left my cell phone aside, and, you know, continue with my life. And the next day, it was crazy. It had exploded in Instagram, it was having so many views, I was getting a lot of people following me. And it was like not really understanding what was going on. But then by reading their messages, I realized that we're all needing to hear that from somebody in Spanish, but they didn't have it, they have nobody telling them that there was sending them to their families. And soon, you know, what used to be a misinformation chain, going between group chats in, in, you know, these population change to be a chain of these video explaining vaccines very simply, and why RNA was not going to kill us. So that was a moment. Very, you know, it's a stressful, but it was very exciting to see that the way I had phrase things was resonating with people, and was making them understand that at least just give them a second chance just give a chance to to understand the vaccines and not say no, automatically. And just, I feel that it was just like a snowball that kept growing. And I kept realizing, you know, I could explain some other things, everything in the level of what you know, people will normally just learn in high school, but maybe they don't remember, you know, what is DNA? What is RNA? What is the protein? What are ourselves? How do they work? So just very simple things that if you don't work in science, and maybe you don't have a passion for science? Well, you just saw that in like, fourth grade biology and then forgot it. But now, it is important again, because you're deciding whether to get vaccinated with something that will, you know, have a just make its work in a set of yourself. So yeah, I think it just kept growing, it kept having a really good response from people and not after that it just transformed into a more general science communication space in Spanish, just because there's not much available.

43:28  
Jim: Oh, I really love that thank you for stepping into that space and, and using your, your, your scientific understanding your biological background to to help others that that's, that's huge. In the path is all about to. And it's wonderful that you were in that place and really had the foresight to invest in this. Guess moving forward? How do you see social media fitting into your professional persona?

44:05  
Juliana: Yeah, that's a question I've asked myself for this whole year and a half. But I think I've come to some things that I value a lot for men. And one is that as scientists, we sometimes get really concentrated on only what we do, specifically our for example, our PATH system, our specific interests, and having a place or having a community that sort of moves me to read about other things, not only what I'm doing and what my close community is doing, but what is happening in you know, cancer, you know, animal research, all these other things, and picking things that are important for people to understand and that because they're impacting their own lives, like in that moment, it was vaccines, but it can also be gene editing. It can also be in GMO was climate change, like there's so many big topics that have a science background behind it. So I feel like it, it's been one of the reasons that have brought me to a moment in my career where I feel very versatile in that I love what I do, I love my research, and I see myself going forward in that direction. But I have like these. I don't know if it's like an alter ego like, side of me, that has a really nice community and can interact with that. And I think the other really valuable thing is that about 82% of the people that follow me on Instagram are women. And they are usually aged between 18 and like 3840. And, you know, from conversations with them from reading their messages, I found out that most of them are just either already in science, and they're doing their own PhDs, their own masters, their own undergrad, or just thinking of going into science. So it has also combined not only the idea of, you know, talking about science to a broad audience, but showing other women and other girls, especially how it looks like to be a women in science, and how it looks like to be, you know, day to day, these sometimes you have like this really unclear idea of how it will look like when you go to the European HD, but if you just open your Instagram, and among all the 1000s, you know, people you follow, there's a few that show you like, Oh, hey, I'm doing a PCR today, and this is what PCRs look like. So that has been rewarding, but at the same sense, it has generated a bigger community for me that I do expect will help me in sort of my own academic path, to have this connections, you know, having both my connections here in the US, the people, you know, my close community aps that has been 100% supportive with me ever since I was an undergrad to now. And then these other community that's all over the world. But it's just opening doors, you know, elsewhere. And I feel like I'm opening one door here, which is this is what it looks like, if you feel like pursuing it. Just this is an example. It's not going to be 100% like that. But just so that you have an image of how it is

47:26  
Jim: Fantastic. That really, it's exciting. There's so many scientists who are using social media these days. And I think you're doing exceptionally well. Thank you so much for for what you're doing in that space. And thank you so much for being our guest today on Plan topia, it's been a real pleasure to have this conversation with you.

47:49  
Juliana: Thank you, Jim for having me. It was a pleasure to be here and thank you all who are listening to us today.

47:55  
Jim: And we just heard from Juliana Gonzalez Tobon from Cornell University talking about her research on small non coding RNAs and the role they play in regulating plant pathogen interactions. We've also talked a bit about her social media presence and what she's doing to fight COVID misinformation and really raise the profile of science, understanding communication more broadly. I'm Jim Bradeen, the host of the Plantopia podcast. Plantopia is a production of the American Phytopathological Society. Thank you very much for joining today and we will see you next time.

Transcribed by https://otter.ai