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An Investigation into the Mechanisms of Dorsal Closure

Dorsal closure is an essential developmental process during embryogenesis in the fruit fly, Drosophila melanogaster. It is preceded by germ band retraction, in which the germ band (made up of the developing germ layers) retracts and exposes the dorsal side of the fly embryo (Fig. 1A). This reveals an eye-shaped opening in the epithelium that consists of a layer of thin, flat cells, called the amnioserosa (Hartenstein et al. 1993, Kiehart et al. 2017). After the germ band retracts, the amnioserosa cells move back and forth, ingress, and destroy themselves while the bordering lateral epidermis sheets move in towards the dorsal midline where they meet and adhere, forming a seamed and then seamless epithelium (Fig. 2). 

[IMG 1]

Fig. 1. Germ band revealing amnioserosa and edgewise epidermal cells. A) Germ band retraction and reveal of the amnioserosa (as). B) Movement of the lateral epidermis to close the dorsal opening (ie. dorsal closure). Image taken from Hartenstein’s Atlas of Drosophila Development.

[IMG 2]

Fig. 2. End of dorsal closure. The two epidermal sheets have met and formed a seam that will soon disappear (Mortensen et al., 2018)

Numerous proteins and signaling mechanisms are involved in tissue movements during development. Studying these processes in the wee fruit fly as a model system helps us to understand these important biological processes in a wide range of mammals. In my project for this summer, I hope to learn more about the molecules involved in dorsal closure. For example, the placement and development of α-actinin in the drosophila embryo is moderated by various proteins, and by tagging the molecules with fluorescent proteins and then imaging them live during the closure process, we are able to gain a better understanding of how these molecules work in both normal development and mutant backgrounds.

References

Hartenstein, V. (1993). Atlas of Drosophila development. Plainview, N.Y: Cold Spring Harbor Laboratory Press.

Kiehart, D. P., Crawford, J. M., Aristotelous, A., Venakides, S., & Edwards, G. S. (2017). Cell Sheet Morphogenesis: Dorsal Closure in Drosophila melanogaster as a Model System. Annual review of cell and developmental biology, 33, 169–202. https://doi.org/10.1146/annurev-cellbio-111315125357

Mortensen, R. D., Moore, R. P., Fogerson, S. M., Chiou, H. Y., Obinero, C. V., Prabhu, N. K., Wei, A. H., Crawford, J. M., & Kiehart, D. P. (2018). Identifying Genetic Players in Cell Sheet Morphogenesis Using a Drosophila Deficiency Screen for Genes on Chromosome 2R Involved in Dorsal Closure. G3 (Bethesda, Md.)8(7), 2361–2387. https://doi.org/10.1534/g3.118.200233

Stronach B. (2014). Extensive nonmuscle expression and epithelial apicobasal localization of the Drosophila ALP/Enigma family protein, Zasp52. Gene expression patterns : GEP, 15(2), 67–79. https://doi.org/10.1016/j.gep.2014.05.002

Calcium Signaling in Arabidopsis Thaliana

My lab was sent Arabidopsis thaliana seeds by another lab and asked to bulk the lines and analyze their phenotypes. In practice, “bulking the lines” entails a lot of plant care: planting seeds on plates, transplanting them to soil, watering, tying up unruly stems, and harvesting tissue. As the plants develop, we try to observe potential phenotypes that change their growth or appearance. Once we harvest tissue, we can genotype the plants. We do this by extracting DNA from leaves, running it through PCR, and then screening them for their tDNA insert. Essentially, we want to double-check that the genotype is actually present for any phenotypes we suspect. The lines we’ve been given that we are most interested in are knockouts such as calcium-dependent protein kinase 3 (CPK3) and CPK6. We screen our PCR products on a gel to see if they return a band for the tDNA insert, and then we’ll move on to imaging tissue.

Calcium is an important signaling molecule in plants, especially in stimulus-response pathways. Many unknowns exist about how calcium works, especially its transduction pathways’ specific, mechanistic details. However, it is suspected that when the plant is stressed or initiating an immune response, CPKs mediate phosphorylation events that increase the rates of stomatal closure, likely through the upregulation of slow anion channels.  Calcium is part of a concert of biomolecules that work toward stomatal closure. Whether calcium signals come before or after other important players in the plant immune response, such as abscisic acid (ABA), has not been determined. Other calcium-independent processes could also be more responsible for the closure of stomata. My project aims to discover as much as possible about the calcium-related phenotype for the mutant lines that we were sent and, in doing so, come to a better understanding of the role calcium plays in the plant immune system and cytoskeletal response (such as stomatal closure).

To accomplish this, we can compare the calcium signaling in wild-type Arabidopsis to the mutant lines we were sent. The plant samples have a  genetically-coded indicator, R-GECO1. This molecule functions as a biosensor, allowing us to pick up on calcium signaling because the R-GECO1 is adapted from red fluorescent proteins (RFPs) that fluoresce when excited by calcium. While imaging under the confocal, as I spoke about in my last post, we can induce an immune response by treating our tissue sample with the pathogen flagellum protein flg22. The result from the microscope is a video where you can see a wave of calcium cross through the plant cells, which we call calcium’s spatiotemporal dynamics. Image processing techniques can be used to gather statistics about the response to quantitatively compare between samples. After we’ve genotyped and screened all samples, we’ll select the most representative ones from each line to subject to further experimentation and see how each mutant line’s calcium signaling behavior differs, if at all, from the wild-type. For example, if the CPK3 knockout line has significantly suppressed calcium signals and resulted in reduced stomata closure, it could be a clue that CPK3 is an important part of the pathway. If the CPK3 mutant and the wildtype have very similar calcium responses under the confocal, it could be that CPK3 is downstream completely of the calcium response.

An ELPnation [Explanation] of My Project

My research project for this summer will be to analyze various elastin-like polypeptides (ELPs). ELPs are polypeptides that incorporate the 5 amino acid long sequence of Val-Pro-Gly-Xaa-Gly, where Xaa represents an unspecific amino acid. ELPs are a kind of artificial intrinsically disordered protein (IDP), which are proteins that do not fold in the typical way but rather maintain an unfolded (disordered) form that permits multivalent behavior. ELPs also change phase with lower critical solution temperature behavior, which means that they will be soluble below a critical temperature and phase separate at/above it.

So far, I have worked on cloning recombinant plasmids that contain part of the desired ELP sequence with E. coli. Each ELP sequence has an “A cut” and a “B cut” plasmid which will be ligated together in order to get the desired sequence. This is done because ELP sequences are quite repetitive and this makes it difficult for manufacturers to directly make it. E. coli is also used in order to generate the protein from the plasmid. Flasks of E. coli are given the plasmid and reproduce until they almost reach carrying capacity, at which point they are given a treatment to induce protein synthesis. This is done in order to maximize yield as a flask well below carrying capacity would not be able to produce as much protein and one at carrying capacity would not be as metabolically active. 

 

Epigenome Editing

The Gersbach lab is home to a variety of projects, the one thing they all have in common is that these projects focus on genetics. My specific project focuses on the genetics behind Prader-Willi syndrome. Patients with this syndrome exhibit a multitude of negative symptoms, but the most known symptom is constant unbearable hunger.

Organisms have a maternal and a paternal copy of every autosomal chromosome, however, these copies are not the same. This means that the maternal copy of the chromosome carries some genetic information that the paternal copy does not. This phenomenon is known as genetic imprinting.

Prader-Willi syndrome is caused by an error in genomic imprinting. In PW syndrome, the patient has a loss of expression in the paternal copy of chromosome 15. However, with epigenetic therapy it may be possible to use CRISPR-Cas 9 to activate the maternal copy of this gene. My mentor is focused on finding the locus in the maternal gene that controls the PWS gene expression.

Gait Analysis in the Animal Locomotion Lab

My research this summer in the Animal Locomotion Lab consists of analyzing humans and their gait during movements such as walking with stiff legs, running, and walking compliantly. For reference, walking with stiff legs is the typical human gait, while walking compliantly is the equivalent of walking like an ape when they walk on two feet. There are three things that the lab is looking at within this one dataset: method validation, figuring out why evolutionarily humans many have developed their signature bipedal walk, and figuring out how to increase quality of life for people who have had parts of their pelvis removed.

One piece of the work with the dataset includes validating the ways that the data was collected in order to make future data collection easier as well as motion capture technology more accessible in clinical settings( where it is underutilized but could be very useful). The current way of capturing force, angle, velocity, and acceleration data for movement analysis was by using a force plate, cameras, and code to digitize each of the markers, and hand analysis. All of these steps are not intuitive to people who are not in the field, require a lot of time, and also require a lot of money and resources to implement. The new way to gather motion capture data is through a program called OpenCap. In order to run this program, all you need is two IOS devices and the OpenCap program.

The second thing that will be looked at with this data is a potential explanation for why humans may have developed the stiff leg walk. We are the only mammals who walk the way that we do, so it is very intriguing to anthropologists to discover both why and how that came about. How is a much more difficult question, so for now, the animal locomotion lab will focus on why it could have happened.  By analyzing the force patterns and loads of how we walk today compared to how out closet ancestors walk, we may be able to find that answer.

Lastly, the data will also be used as a comparison for patients who have had parts of their pelvis removed. Analyzing their gait will lead to answering questions about how surgeons and physical therapists can cater their care to these patients and better their quality of life.

Sleep disruption due to prenatal environmental toxin exposure and neurodevelopment disorder pathology

The prevalence of neurodevelopmental disorders (NDDs), such as Autism Spectrum Disorder (ASD) and Attention Deficit Hyperactivity Disorder (ADHD), has increased rapidly over the past two decades. As such, much research has gone into the root causes and mechanisms of these disorders. Previous studies on the genetic roots of NDDs have identified several alleles associated with NDD pathology, however, prenatal environmental stressors and toxins are thought to contribute greatly to this recent increase.

Sleep plays a critical role in synapse remodeling, especially during adolescence. Astrocytes, a type of glial cell essential to regulating neuronal activity, have recently been shown to modulate the sleep-wake cycle. Specifically, astrocytes seem to regulate both depth and duration of NREM sleep. Previous work has shown that sleep appears to be particularly sensitive to environmental stressors and toxins. 

In the case of neurodevelopmental disorders, such as autism spectrum disorder, sleep disturbances are observed in nearly 86% of patients. Thus, the project I will be working on this summer aims to investigate the mechanisms by which prenatal exposure to environmental toxins impacts the development of neurodevelopmental disorder pathology. 

In my mentor’s previous work, she identified that a prenatal combined diesel exhaust particle and maternal stress (DEP/MS) paradigm results in neurodevelopmental disorder pathology in offspring. 

Using this mouse model, we plan to address two main questions. Firstly, how does prenatal exposure to maternal stress and environmental toxins impact sleep patterns in offspring? Secondly, do we observe changes in gene expression patterns and astrocyte physiology in the brains of these mice?

We’ve begun by using electroencephalography (EEG) and electromyography (EMG) to analyze sleep patterns in DEP/MS mice offspring. By doing this, we hope to determine how time spent in NREM and REM sleep differs between control and DEP/MS mice. We then plan to isolate RNA from frontal and parietal cortical astrocytes in order to analyze gene expression patterns through quantitative real-time PCR. Additionally, building on the sex differences in NDD pathology observed in my mentor’s previous work, we plan to use the forced-swim test to measure depressive behavior in DEP/MS mice.

Decoding Cellular Dynamics in Chlamydomonas reinhardtii: Unveiling the Role of ARC6

In my research project, I delve into the fascinating world of Chlamydomonas reinhardtii, a unicellular green alga that serves as an excellent model organism for studying cellular dynamics. This organism is special in that it divides by furrowing, yet doesn’t have a contractile actomyosin ring. I am focusing on unraveling the intricate role of ARC6, a key divisome protein, by characterizing its localization within the cell and generating reporter strains through crosses to enhance our understanding of different phenotypes. Through this exploration, I aim to shed light on the fundamental mechanisms governing cellular processes in this model organism.

One of the primary functions of ARC6 is its involvement in the assembly and maintenance of the division site during cell division. By interacting with other cytoskeletal proteins, such as actin and tubulin, ARC6 ensures proper positioning and organization of the divisome proteins, facilitating successful cell division. Additionally, ARC6 is implicated in the formation and maintenance of other microtubule structures, contributing to the overall cytoskeletal architecture of the cell. ARC6 has also been implicated in various cellular processes in Chlamydomonas reinhardtii. ARC6, a conserved protein, plays a pivotal role in various cellular processes, including cytoskeletal organization, membrane trafficking, and organelle biogenesis. It associates with endosomal and Golgi membranes, modulating the transport and fusion of vesicles within the cell. These interactions highlight the role of ARC6 in regulating intracellular trafficking pathways, ensuring efficient delivery of essential molecules to their designated destinations. 

However, its precise localization within the cell remains to be fully characterized. By employing microscopy techniques and fluorescent tagging methods, I will investigate the subcellular distribution of ARC6. Unraveling the specific compartments in which ARC6 resides will provide crucial insights into its functional relevance and its potential role in cellular processes.

To further enhance our understanding of ARC6 and its involvement in cellular dynamics, I plan to conduct crosses to generate different reporter strains. These strains are designed to carry specific markers or tags that allow us to visualize and track ARC6 in various cellular contexts. In addition to localization studies, my research project also involves characterizing mutant phenotypes associated with ARC6. By generating mutants with specific alterations or disruptions in the ARC6 gene, we can explore the impact of these mutations on cellular dynamics and identify any resulting phenotypic changes. Through careful observation and analysis, we aim to uncover the functional significance of ARC6 and its contribution to the overall cellular architecture and function of Chlamydomonas reinhardtii.

 

Marco Polo: How Do Lichen-Forming Fungi Find Their Cyanobacterial Partners?

This summer, I will compare lichenized cyanobacteria communities to environmental cyanobacteria communities (cyanobacteria living outside the lichens) to inform how lichen-forming fungi associate with their cyanobacterial partners. For context, lichens are organisms made of symbiotic associations between algae/cyanobacteria and fungi. Fungi in lichen can reproduce sexually via fungal spores, which are essentially sterile, free of cyanobacteria, and it is largely unknown how the fungi find and associate with their symbiotic partners. In nature, fungal species have been observed associating with different cyanobacterial species, sometimes “switching” between cyanobacterial partners. The mechanism behind symbiosis formation is unclear; it is unknown where and how often the fungi find their cyanobacterial partners, and we want to know if the same cyanobacteria are found in the surrounding environment. 

My project focuses on lichens made of Peltigera, a genus of lichen-forming fungi, and Nostoc, a genus of blue-green algae or cyanobacteria. Using lichen and environmental samples, we want to ask: are lichenized cyanobacteria similar to, or different from, the environmental cyanobacteria found outside the lichens? The Lutzoni Lab collected lichen and environmental samples across Alberta, Canada, to help answer this question. The lab collected roughly 2500 lichen samples and 1800 environmental samples across 15 sites spread over five natural regions of Alberta (3 sites per natural region). The environmental samples consist of substrate sampled next to and between lichens and are split into 900 “top” and 900 “bottom” samples. The top samples were collected closer to the earth’s surface, and the bottom samples were collected deeper underground. 

This summer, I aim to answer two primary questions to determine the best method for extracting and sequencing the Nostoc DNA from lichen and environmental samples!

First, we want to know if the 16S rRNA or rbcLX gene is a more accurate marker for detecting Nostoc in the samples. The rbcLX gene is more specific to cyanobacteria and has more variation than the 16S rRNA gene, so it could more accurately classify between species of Nostoc. However, Nostoc contain one copy of the rbcLX gene compared to multiple copies of the 16S rRNA gene. The environmental samples may have low abundances of Nostoc, so sequencing the 16S rRNA gene may be more suitable for detecting the low cyanobacteria levels. To answer this question, we are testing the 16S rRNA and rbcLX approaches on 12 environmental samples which have already undergone metagenomic and metatranscriptomic analyses. By comparing the resulting 16S rRNA and rbcLX sequences to pre-existing data, we will select the marker with which we will sequence the remaining environmental samples. We hypothesize that 16S rRNA will more accurately detect the Nostoc because we are trying to detect microbes presumably in trace amounts, and because the 16S rRNA gene is the standard marker in microbiology. 

Next, we want to determine how the cyanobacterial communities in the top environmental samples compare to those of the bottom. As mentioned above, the 900 top and 900 bottom samples are from the same areas but different depths into the substrate. We want to see if the bottom cyanobacterial communities are a subset of those of the top samples, and if so, only extract DNA from the top samples to save time and money. We hypothesize that the bottom samples will be a subset of the top, and more Nostoc will be detected in the top samples because Nostoc require sunlight to photosynthesize ☀️

Lots and lots of lichen samples! 6/14/23

L1 Arrest and Abnormalities in C. elegans

This summer, I’m working in the Baugh Lab studying the roundworm Caenorhabditis elegans and the effects of L1 arrest. 

C. elegans larvae that hatch into an environment without any nutrients are arrested in the first larval stage of development (L1). This means that they simply do not grow, and they can remain in this stage for weeks. Once they receive enough food, they can resume development as normal. 

However, extended L1 arrest can lead to abnormalities in adult C. elegans, just as early-life starvation can cause later problems for humans. Starved worms are more likely to develop issues that interfere with reproduction, including germline tumors and uterine masses. My project investigates potential genetic causes for these abnormalities. 

Previous results from my mentor, Ivan, indicate that the C. elegans endogenous RNAi pathway may regulate the abnormalities. RNAi stands for RNA interference, and is a mechanism used to regulate gene expression. Cells recognize double-stranded RNA (often foreign), cut it up, and incorporate it into a protein complex. This complex uses the RNA to recognize specific mRNA molecules, which it binds to and cleaves, preventing them from being translated into proteins. RNAi is used for regulation within the cell and to protect cells against viruses, but is also often leveraged for research, as it can be used to specify and turn off genes. 

Right now, I’m primarily looking into genes that code for proteins involved in the RNAi pathway. I’ll be examining the frequency of abnormalities for worms that have certain genes turned off either by mutation or exogenous RNAi. So far, I’ve been maintaining different mutant strains and preparing RNAi, which is delivered to C. elegans through their food. Soon, I’ll be scoring the abnormalities for each strain and RNAi group, and figure out where to go from there!

A Summer of Exploring Epilepsy

Hello dear readers!!

This summer I’m very excited to be reporting on my experiences researching epilepsy with the McNamara Lab. I’ve actually been working in this lab since November 2022 as an undergraduate intern, and have loved taking a hands-on approach to exploring neuroscience as it’s one of my favorite branches of biology!

To elaborate more upon what my lab hopes to achieve with its research, it’s been established that seizures themselves can be a cause of epileptogenesis, a phenomenon attributed to the BDNF receptor tyrosine kinase, or TrkB. Unexpectedly, it has also been discovered that briefly inhibiting the binding of BDNF and TrkB caused epileptogenesis to not only stop but actually regress, but this only occurs when the binding is inhibited following a seizure. Given this new proposal that seizures can also be protective against epileptogenesis, my project will consist of investigating the mechanisms behind these protective pathways, and my job will shift towards applying in situ hybridization to measure the expression of relevant mRNA sequences in hippocampal neurons.

From this summer research experience I’m not only hoping to acquire additional technical lab skills such as RNAScope through my project, but I’m also excited for the collaboration that will occur in the lab with mentors and through the program’s faculty seminars and professional development workshops. This program will teach me more about conducting research and then presenting my findings in a way that’s communicable to a wider audience through the final research showcase.

My responsibilities from last semester have consisted of digesting mice tails to extract DNA, running PCR gels to genotype the different lines of mice used in a variety of experiments, and cryosectioning mice brains for analysis. As for my first week back on the job, I’ve split my time between reading up on this new branch of epilepsy research I’m about to undertake, organizing the tails in the freezer that have accumulated in the month I’ve been gone, continuing to run a few PCRs and gels, and I’ve begun to play around with ImageJ to develop a protocol we can use to analyze the results of our in situ hybridizations. Finally, this Thursday there was a cute Farmer’s Market at the Medicine Pavilion Greenway where I bought some flowers, and we got to have a lovely lunch with the whole lab on Friday!

Thanks for stopping by my blog!

Until next week,

Emma Podol

 

Reflection on the summer

Before the program started, I set the goals of “practicing how to think and tackle problems like a researcher and figuring out whether doing basic science research is what I want.” As the program comes to an end, I’m starting to realize my most important takeaway is that I love being a student. Students learn the answers to questions. Scientists are but a special kind of student. They can’t find answers in a textbook or from a teacher, but they must seek answers from the natural world itself. Choosing a career in research would mean becoming a life-long student. It’s exciting, intellectually stimulating, and rewarding. Before BSURF, I often said that I’m interested in research. Now, I’m certain that research will be a part of what I do in the future. 

One other thing I would mention is that this program has provided numerous opportunities for practicing how to communicate science. How much communication is involved in a career in science is also something I didn’t understand before. In addition to doing research in the lab, I really enjoyed the seminars and workshop sessions that this program offered. Finally, I would like to thank Rachel, Dr. Ko, members of the Ko lab, Dr. Grunwald, Dr. Harrell, and Austin for making this wonderful experience possible.

Launching my career in science

In retrospect, this summer research experience has been extremely fulfilling. Before I began working in the lab, I set a goal for myself: I wanted to become more confident in my research abilities. This “confidence” does not only include my confidence when conducting experiments but also confidence when sharing my research with others. Through the chalk talks, conversations with peers and family, and the poster symposium, I can feel that I have accomplished this goal; I have become a better speaker in communicating my science. It is truly gratifying to know that I have grown so much in just two months. Additionally, this summer’s research helped me recognize and refine my strengths. I also evolved by acquiring knowledge in a field I once knew nothing about.

Not only did I transform this summer, but my definition of research has also evolved. Prior to this experience, I knew research involves working in the lab and conducting experiments. But after this experience, I can confidently say that research is much more than that. Research involves creativity, insights from others, collaboration with coworkers, and innovative ideas. My colleagues in the lab and the faculty have all given me words of wisdom that I will apply in my life. I truly enjoyed my experience in the lab, and even though this B-SURF experience has ended, I know that this experience has launched the beginning of my career in science.

A Great Summer With BSURF

BSURF was a wonderful experience. When first hearing about and applying to the program, I had no idea what to expect from a sumer research experience. I knew that I wanted to try something with biological and virological research in my time at Duke but had no idea how to get involved or how to find the right lab and mentor to help me get a good experience. In hearing about BSURF, I learned that this program would help to navigate this confusing process and give more experiences on how research works and how to be a good researcher. I was very excited for this type of opportunity even though I did not know what to actually expect in the research itself.
Now at the end of BSURF, I can happily say that BSURF was everything it promised and more. I was able to join a lab in virology that helped me to better understand what research in virology and microbiology is through the help of wonderful mentors. I was able to get good advice from both my mentors in my lab, Vanessa and Dr. Horner, and the leaders of the BSURF program, Austin, Dr. Harrell, & Dr. Grunwald. I was able to make great friends with other students interested in biological research and spend lots of time discussing research and other interesting topics with programmed events. I am very glad that I was able to be a part of this experience!

When all was said and done

In my first blog post (written what seems like both eons and mere days ago), I emphasized the role that uncertainty plays in becoming a more active learner and better scientist. Instead of shying away from uncertainty, I expected to become comfortable with it, to the point that when I left BSURF, I would do so with a greater appreciation for challenges and my own capabilities.

Indeed, over the course of the program, I found myself in situations that ultimately strengthened my resolve about my academic and professional goals. Through the faculty talks, the chalk talks, the grad/MSTP student panel, and the poster sessions, I was able to hear about only a fraction of the science going on around me here at Duke. While the thought is a little overwhelming when it comes to the breadth of opportunities for engaging said science, it’s also heartening. I have been able to narrow down what concepts I want to continue to investigate, the types of questions I want to ask, and the community I want to be surrounded by. Thanks to my time in my lab, I have learned some of the technical skills that will enable my scientific pursuits and furthered my comprehension of cell biology. As such, I greatly appreciate my time in BSURF and hope to continue this growth throughout the rest of my time at Duke.     

That’s a wrap on BSURF!

After the conclusion of the poster presentation for BSURF, I decided to reread my very first blog about my expectations of the summer. These past 8 weeks have flown by, yet the Amelia writing the first blog seems so different. She was just at the beginning of her journey to being a researcher, with so much ahead of her. 

I am truly amazed by how much I have learned throughout this program. I started out with very little programming skills and now that we’re the end of BSURF, I am comfortable with coding for the whole work day, and I was able to complete my goals for my project! I must admit, there were many times where I was overwhelmed by all of the troubleshooting and debugging I had to work through, as well as maneuvering my way through a new language, Python. Thankfully, I was able to push through, majorly thanks to the help of my amazing mentors Anne and Liz, and my fellow lab mate Chris. Overall, I was pleasantly surprised by how welcoming everyone was at the Pearson Lab. It made my summer research experience even more enjoyable. I’d also like to give a huge thanks to John for giving me the opportunity to join the Pearson Lab for the summer.

I could go on and on about how rewarding this experience was, but before I wrap up this final blog, I would like to thank everyone who is a part of BSURF. Without Dr. Grunwald, Dr. Harrell, and Austin, this experience would not be nearly as great as it has been. I always looked forward to your smiling faces in the mornings and Dr. Grunwald’s jokes throughout the day. The BSURF excursions were some of my favorite memories of the summer – canoeing, dinner at Dr. G’s house, the Lemur Center, the art gallery crawl, just to name a few. Last but not least, I really enjoyed the community of bsurfers and I’m lucky to say that I made some amazing new friends along the way. I wish you all the best of luck with your future research endeavors! 

Comprehensive BSURF Review

What exactly is research? Research is pushing the boundaries of knowledge and venturing to uncharted territory. It’s experiencing failure while logically and creativity exploring new angles to tackle the problem. Research is a lifestyle, but is it a field I am capable of pursuing? That was the question that I had before this summer.

If I had to summarize BSURF in one word, it would be insightful. I held an apprehensive outlook on research. I construed it as an arduous field requiring years of knowledge before even considering collaborating with others; however, working on a well-funded lab this summer unveiled the fallacy of my aforementioned perspective. My eight weeks with the program illuminated on the pleasurable, intellectual, and collaborative challenge that is called research. Diving deep into a subject was amazing, especially receiving advice from knowledgable peers and professors. I had forgone my hesitance to reach out to more informed persons and altered my self-efficacy in pursuing research.

Overall, the community and experience have illuminated on an amazing path that I had previously disregarded with minimal consideration. Now, I look forward to continuing with research in my upcoming and future years, and hope to continue with research even after I complete my undergraduate degree. Thank you BSURF for the memories. I will be leaving with new friends, insight, skills, and a deeper understanding of my goals and interests.

 

BSURFun in the Sun!

What a summer. I originally applied to BSURF because I wanted to explore my options with biological science research and career pathways – and that is absolutely what was fostered through this program. These eight weeks have absolutely flown by, with all of the research, meetings, and fun activities that makes BSURF such a unique experience. From canoeing on the Eno River and climbing the Duke Chapel, to eating popcorn for breakfast and having late night hangouts in Swift Apartments, I have thoroughly enjoyed my time here this summer. And of course, this program would not be what it is without the invaluable knowledge and expertise I gained from my research and weekly seminars. I treasure the growth I have experienced in just two months, as well as the friends I have made along the way (and who will remain so).

I really appreciate this wonderful opportunity, and I could not imagine having done anything else for my summer. Being surrounded by my extremely qualified and caring peers created an exceptional learning environment, filled with discussion and also fun and laughs.

Thank you BSURF for making my summer so extraordinary and for connecting me with friends, mentors, researchers, and faculty that truly care about undergraduate research and bettering society with science. Thank you for allowing me to explore and branch out. I am honored to be a Biological Science Undergraduate Research Fellow.

(and now, if you ever need someone to identify aquatic macroinvertebrates for you, just call me up!)

The Beginning of an Era

This summer has taught me at least one thing: eight weeks is not much time at all. I never understood the “slow” pace of research. The idea of working on a project for years was strange to me; I never could wrap my head around why so much time was needed. Now, reflecting on what has been the quickest summer I remember, I understand that my research experience was a very short one, and I want more.

Overall, this summer in the lab has been a great experience and has altered my desired career and academic paths. I came into Duke as someone who was very unsure about how to channel my love of science. I considered many paths, including that of a pure PhD scientist or physician scientist, but eventually decided that my place was in patient care with limited involvement in research. I didn’t like the idea of being in an office or not having contact with other people (things that I thought were hallmarks of a career in research).

This summer showed me that I truly love the process of research and scientific inquiry. I love asking questions, understanding and applying techniques and knowledge, and being able to do those things in service of my other passion, patient care, is truly a wonderful thing. When I ruled out a career in research, I really didn’t have enough of an idea of what it was actually like. I just knew it was not as much of a concrete path as a career as an MD can be. I didn’t know how collaborative, social, and fun the lab environment could be.

I’ve now reconsidered what I want. I know that I want to do research in some major capacity. I’m not yet sure if that would be as a PI or an associate of someone else’s lab or in industry, but I do think that I would be more fulfilled by a career in research and patient care than in either alone. Going along with that goal, I am once again very strongly leaning towards pursuing a Medical Scientist Training Program. This summer has shown me how much I love the lab and convinced me that I could be happy despite being in school for all of my 20s. I truly cannot wait to spend more time in lab and get to properly follow a project, maybe even one of mine own, from beginning to end.