Undergraduate Research Magazine with Proceedings of the Biological Sciences Student Research Showcase 2018
Volume 9 2018-2019
letter from
THE EDITOR
A humanistic approach to the scientific method has long been considered a juxtaposition, a contrast of fields that are not typically found in conjunction. Yet, accessibility to science is only hindered by such a limitation. Year after year, the staff behind Under the Scope breaks this barrier between the humanities and the sciences as they work together to integrate art, literature, and science in a product directed toward readers who do not necessarily have a biological background. Every page of this magazine begins as a blank slate, and there is nothing but possibility in the empty pages at the start of the new year. With every successive word the writers contribute, every illustration our artists create, every image our photographers capture, and every design element our production staff incorporates, the blank page is slowly filled to the brim with a beautiful mixture of creativity, talent, and a love for biology. Science is dependent on not only constant progress but progress across the wide variety of specializations within the field. Just as multiple academic fields are brought together in Under the Scope, biology in all its specializations is also united through the diverse range of articles written. From decoding the brain in sensory processing and neurodegenerative diseases to clarifying the implications of cancer to magnifying the microscopic immune system, the articles are comprehensive. Our writers have spent countless
hours interviewing, drafting, and honing outstanding pieces that highlight many different aspects of biology. The vivid illustrations and photographs that accompany them serve as indispensable companions to the words, allowing the reader’s imagination to bring abstract biological concepts to life. Under the Scope is a publication accessible and comprehensible to the general public. It therefore serves the unique role of featuring some of our brightest undergraduate researchers and spreading awareness of advancements in biology while simultaneously building a foundational knowledge of the field for its audience. Integrating an interdisciplinary approach to scientific communication, our staff members act as undergraduate ambassadors for biology with their incredible talents every year. With great honor and pleasure I present to you Under the Scope, Volume 9. It is my hope that every article inspires you as it did me. Regards,
Tushara Govind
Executive Editor, Under the Scope
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Top Row: Alejandro Dauguet, Daniel Lutz, Anne Marie Berry, Mark Jacob, Jialin Xu, Michael Kalisz, Sam Zilberman
FACULTY ADVISORY BOARD
2nd Row: Soha Khalid, Jenny Chiem, Sneha Ganguly, Shreya Shriram, Sanjana Sharma, Shae Galli, Melody Nazarbegian, Meera Patel, Nikhil Jampana
Carolyn Kurle, Ph.D.
3rd Row: Lisa Chik, Andra Thomas, Vickie Kuo, Salma Sheriff, Maya Gopalakrishnan, Alexandra Babakanian, Megan Griswold, Katie Clark, Gayathri Kalla, Andrea Pednault, Cristina Corral, Michael Endow Bottom Row: Tushara Govind, Arya Natarajan, Theresa Bui, Victoria Hoznek, Rebecca Hu, Serena Tan, Liam Huber, Cassidy Lam, Tiffany Huynh, Emma Huie, Lauren Brumage, Ashni Vora, Samreen Haque, Sharada Saraf
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Suckjoon Jun, Ph.D. Chih-ying Su, Ph.D. Jim Wilhelm, Ph.D. Ella Tour, Ph.D. Elsa Cleland, Ph.D. Jill Leutgeb, Ph.D. Lisa McDonnell, Ph.D. Special thanks to John Tat, Ph.D. for editing and advising assistance
HEAD ADVISORS
CORE STAFF EDITORS
WRITERS
James Cooke, Ph.D. Assistant Teaching Professor of Neurobiology
Sharada Saraf
Xaver Audhya
Lisa Chik
CJ Hattori
Lauren Brumage
Vickie Kuo
Liam Huber
Belinda Tan
Dominique Sy
Ahsan Usmani
Cassidy Lam
Tvisha Devavarapu
Emma Huie
Andra Thomas
Saksham Gupta
Allison Kifer
Hermila Torres Manager, do/Bio Center
EDITORIAL BOARD Executive Editor Tushara Govind
STAFF
Michelle Lin Julia Tu
Features Editor Ashni Vora Production Editor Arya Natarajan Features Design Editor Laura Zhang Head Technical Editor Rebecca Hu Technical Editors Andrea Pedneault Salma Sheriff Alejandro Dauguet Juliana Fox
PHOTOGRAPHERS
COVER ILLUSTRATION
ILLUSTRATORS
Michael Endow
Vicky Hoznek
Vicky Hoznek Varsha Rajesh
Tak Yung Lee
Cristina Corral
Mark Jacob
TABLE OF CONTENTS ILLUSTRATION
Sam Zilberman
Corly Huang
Shae Galli
Katie Clark
Anne Marie Berry
Fiona Halder Michael Kalisz Corly Huang
Ta b le o f C on te nt s 8
NOT TO SCALE: HOW MICROSCOPIC ASPECTS OF THE IMMUNE SYSTEM AFFECT US ALL ALLISON KIFER & BELINDA TAN
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THE BRAIN’S FAVORITE CARNIVAL GAME VICKIE KUO & JULIA TU
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CANCER: ONE SIZE FITS SOME XAVER AUDHYA & ANDRA THOMAS
MAINTAINING THE BRIDGE TO THE BRAIN AHSAN USMANI & TVISHA DEVAVARAPU
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BIOLOGICAL SCIENCES STUDENT RESEARCH SHOWCASE 2018
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NOT TO SCALE: HOW MICROSCOPIC ASPECTS 0F THE IMMUNE SYSTEM AFFECT US ALL
W
hat comes to mind when you think about the immune system? Maybe your first mental image was of you cringing when someone sneezed nearby, knowing those germs could send you spiraling into several weeks’ worth of sickness. Or maybe you imagined diseases spreading like an apocalyptic plague in dystopian novels. Our minds might be imaginative, but how do the miniscule parts of our actual immune systems help us not only to survive, but to add to our quality of life? As a society, we can easily oversimplify the nature of such an intricate system and, in turn, fail to grasp its subtleties. Indeed, fully understanding the art of the immune system is an integral part of our environment and well-being.
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the discovery of three essential proteins for a normal functioning immune system Let us begin with the inner framework of the immune system. In reaction to foreign molecules invading the body, the immune system recruits two main types of responses: innate and adaptive. The innate immune system serves as the body’s first line of defense. It produces natural killer cells and phagocytic cells in order to neutralize invading foreign molecules. The adaptive immune response is more targeted and is initiated when a specific antigen (a foreign substance) is detected by T cells, which are white blood cells that kill infected cells. The adaptive immune system in and of itself is split into sub-systems: cell-mediated and humoral responses. The main difference between these two subtypes is that the humoral response relies on B cells secreting antibodies that bind to foreign antigens to recruit helper T cells for attack. In contrast, the cell-mediated response directly recruits phagocytes and killer T cells to kill the invading antigens.
WR ITT EN BY Allison Kifer & Belinda Tan PHO TO BY Tak Yung Lee ILLUS TRAT IONS BY Varsha Rajesh
Photo: Visualization of immune cells (purple) engulfing pathogens (green). Special thanks to Dr. Zbigniew Mikulski at the La Jolla Institute for Immunology for kindly offering his time and expertise to create this photograph.
UC San Diego students Tomomi Yoshida, Yuya Zhao, and Ciara Alejandra Alvarez-Malo sought to expand the current understanding of adaptive immunity by studying molecules that play key roles in this system. Yoshida discovered a protein that is integral in the adaptive cell-mediated immune response, whereas Zhao found a molecule that is required for a normal humoral response. While studying plant immunology, Alvarez-Malo discovered that circadian rhythm heavily affects the regulation of a plant’s susceptibility.
ZEB2 REGULATES THE MAINTENANCE OF EFFECTOR MEMORY T CELLS Memory T cells are a subset of killer T cells that can recognize and attack pathogens that have invaded previously in order to mount a faster immune response than that of an invasion from a ‘new’ pathogen. When a killer T cell comes into contact with an antigen, it proliferates and can kill infected cells. In most cases, after killer T cells have cleared the pathogen, they undergo apoptosis, or programmed cell death. Interestingly, a population of killer T cells survive and can differentiate into effector memory T cells. As of today, little is known about the mechanism that regulates the formation and maintenance of memory T cells. Undergraduate researcher Tomomi Yoshida from the Goldrath Lab has always been fascinated by how the diverse immune cell types work together to initiate a response to specific pathogens. Thus, for her senior
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thesis project, she studied how a certain type of killer T cell establishes and maintains a population of memory T cells, which helps to provide lasting immune protection against pathogens. Thus, Yoshida sought to explore the mechanism behind memory T cell formation. Yoshida investigated the mechanism of T cell differentiation by focusing on transcription factor Zeb2, which controls killer T cell differentiation. In particular, Zeb2 has been found to be highly expressed in effector memory T cells at later stages of infection. She spent six months making a Zeb2 knockout mouse model to study how Zeb2 regulates the maintenance of CD8+ T cell (a type of killer T cell) without affecting its cell differentiation. She found that when Zeb2 was deleted in CD8+ T cells, the effector memory T cell population went down, suggesting that this factor is key to maintaining stable levels of these cells. Understanding the role of Zeb2 in T cell differentiation adds to our knowledge of the cell-mediated immune response, and may even inform us of how to better develop vaccines that can elicit robust B and T cell responses, which provide lasting protection. Nevertheless, this is just a small piece of the puzzle of how the adaptive immune response works. There is more to be discovered regarding the mechanism for the formation and maintenance of memory T cells and other immune cells.
RIAM’S MEDIATION OF HUMORAL RESPONSE TO T-INDEPENDENT ANTIGENS While Yoshida found a protein that is required for a normal adaptive cell-mediated immune response, researcher Yuya Zhao from the Cantor lab sought to study the immune system from another segment of the adaptive immune response—the humoral response. In order to uncover what exactly regulates lymphocyte proliferation, Zhao studied a protein called Rap1-GTP-interacting adapting molecule (RIAM). It has been shown that germline RIAM knockout mice have a disrupted humoral immunity, and by extension, T cell-specific RIAM knockouts have disrupted T cell activation.
Without the presence of the transcription factor Zeb2, effector T cells and consequently, memory T cells decrease in quantity.
In her study, Zhao knocked out RIAM in B cells to see how the absence of RIAM affects the humoral immune response. Interestingly, the absence of RIAM didn’t disrupt the T-celldependent response—a humoral response that involves T-cell action—but did disrupt that toward both T Independent antigen 1 and 2. A possible explanation for this could be that loss of RIAM causes defects in antibody production, but T cells expressing RIAM may be able to activate B cells and rescue the T-dependent humoral response. This suggests that RIAM expression in B cells is required for a normal T cell independent humoral (response).
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HOW THE CIRCADIAN CLOCK AFFECTS PLANT’S LIFE EXPECTANCY Yoshida and Zhao explored the maintenance and response of elements of the human immune system, but how does this research align with the study of other organisms? Graduate researcher Ciara Alejandra Alvarez-Malo worked with Dr. Jose Pruneda-Paz to explore immune regulation of a fundamental staple in our diets plants. In order to convert sunlight into energy, plants must expose themselves to harmful microorganisms during the daytime. To combat this vulnerability, plants employ their immune system during the day to prevent pathogens from invading. Thus, a plant’s immune response is determined by its circadian rhythm, meaning that the period of time in which a pathogen attacks is pivotal to whether a plant’s immune system can fully defend itself. The nature of plants’ immune response is complex; however, the inner workings of a clock can reflect plants’ intricate pathways rather easily.
The immune responses of plants follow a daily cycle known as the Circadian Clock.
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We know clocks work due to a series of gears that turn to make the second, minute, and hour hands rotate to tell time. Within that system, there are smaller gears that control the rate at which each hand moves. Similarly, in a plant, there are mechanisms that affect the rate of gene expression, much like these smaller gears. If circadian genes like Nonexpressor of Pathogenesis Related Genes 1, or NPR1, are
repressed, it is as if one of the gears of the clock has been jammed. The immune response halts and pathogens are able to successfully attack. Alvarez-Malo’s interest in NPR1 led her to ask: what kind of reciprocal relationship does NPR1 share with circadian regulation and how does this affect immune responses? Since NPR1 expression is time-dependent, Alvarez-Malo found that NPR1 allows certain windows for pathogenic attacks, during which limited NPR1 expression lessens the regulation of the defense response. Furthermore, the different intervals of NPR1 expression cause the mediation of circadian defense responses. Thus, if NPR1 is inhibited, there would be no beneficial regulation of the immune response. But how are circadian clocks within plants relevant? Since we know from Alvarez-Malo’s findings that the circadian clock regulates an immune response, researchers can now search for the exact window of time during which genes like NPR1 fail to mediate immune regulation, and adapt agricultural methods accordingly so as to limit pathogen infections. Crop yield could significantly increase if fewer plants fell prey to pathogens, of benefit to both farmers and consumers.
CONCLUSION The work done by the three aforementioned researchers paints a complex picture of the immune system. Collectively, they found that the Zeb2
transcription factor seems to be required for a functional cell-mediated immune response, while RIAM is required for a functional humoral response. One mutation in any of these elements may cause malfunctions in the immune system, which helps us fight off pathogens, whether newly exposed or previously invaded. Moreover, pathogenic time of invasion is also crucial, as seen in the immune response mediated by the circadian clock gene NPR1. Though all of these areas of research focus on different biological aspects, test organisms, and molecular mechanisms, they are inherently relevant to our day-to-day lives. By studying the immune system in both plants and animals, we are slowly unravelling these complicated systems and learning how to harness their versatile power. Just in 2018, medical researchers have improved immunotherapy techniques that help fight off cancer-inducing tumors. Whether it be our bodies’ response to disease, the medicine we take, or the food we eat, we can owe our understanding of our health to researchers like Yoshida, Zhao, and Alvarez-Malo.
WR ITT EN BY Allison Kifer & Belinda Tan Allison is a Molecular Biology and Literature & Writing double major graduating in 2021. Belinda is a Biochemistry & Cell Biology major graduating in 2020. sqonline.ucsd.edu •
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THE BRAIN’S FAVORITE
CAARRN C NIIV IVVAALLG CARNIVAL GAME GAAM MEE
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the mechanisms behind sensory processing to inform the development of neurodegenerative disease treatments
ing ping ping! The collection of cheerful sights, smells, and sounds at the local county fair shoots your senses into overdrive. Yet, despite all of the commotion, you can easily find your favorite classic carnival game: Roll-A-Ball. Similar to skeeball, this game features a ramp for players to roll their balls into holes arranged in a triangular formation of varying point values. Players direct their balls into holes of higher point values to move their marker closer to the finish line for a prize. Aiming objects toward different destinations also describes sensory processing, a biological system in which neurons send signals toward different areas of the brain to allow for cognition. Defined as our five senses work together to produce a holistic perception of our environment, sensory processing is the nervous system’s interpretation of sensory stimuli, detectable changes in our environments. Sensory stimuli, like the smell of popcorn at a carnival, the sounds of the vendors
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calling, and the sight of neon flashing lights, are integrated and processed by the brain, in order to form effective behavioral responses like choosing to buy popcorn over cotton candy at the fair. Due to the sheer volume of sensory stimuli, the rate at which sensory processing occurs is astonishing and essential for our ease and survival. Failure to receive or process this information correctly can lead to the brain’s inability to properly receive and react to sensory stimuli. This is the basis of sensory processing disorders such as autism, which have a broad spectrum of severity. These Sensory Processing Disorders (SPD) impact approximately ten percent of school-aged children. Recent studies show that biological factors, specifically brain structure, are responsible for sensory processing disorders in children. Developing preventative strategies and medical treatments for such disorders depends on a proper understanding of sensory processing.
BY WRITTEN Tu o & J u li a u K ie k ic V PHOTO BY Katie Clark ILLUST RATIO NS BY Vicky Hoznek
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The cerebral cortex is the brain’s hub for high-level sensory processing. Within the cerebral cortex lies the neocortex, a hotspot for sensory processing research. With six layers and four lobe divisions, the neocortex performs higher function controls, including spatial reasoning, motor commands, sensory perception, language, and conscious thought. The temporal lobe, which is responsible for sound sensory processing, contains the primary auditory cortex (A1). The A1 houses neurons that characterize sound by volume, location, and pitch. By responding to the sound’s intensity, frequency, and timing, neurons in the A1 layer allow for essential functions such as spatial and sound discernment. A1 researchers investigate the mechanics of the relationship between the brain’s chemical health and ability to process sound stimuli.
THE FRAMEWORK
The cerebral cortex is divided into four lobes: frontal lobe, parietal lobe, occipital lobe, and temporal lobe. Together, these four lobes allow for sensory perception and integration.
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The most fundamental part of Roll-A-Ball is the ball’s movement. Each player is given a plastic ball whose hole landing determines how far the player’s marker moves in its path. Similar to aiming and rolling a ball into a hole, the A1 layer receives sensory information from pyramidal neurons and sends a response signal to a specific part of the brain to affect a behavioral outcome. However, uncertainties remain as to where the transmissions of different auditory information go; this is similar to Roll-A-Ball, where players aren’t always sure which hole their ball will enter. Due to the range of appropriate targets including the thalamus, inferior colliculus, amygdala, and the striatum, it is still unclear whether A1 projections are always sent
to multiple targets or whether these projections could distinguish their targets based on specific auditory information. Tackling this question is student researcher Mandy Lai of the Isaacson Lab at the UC San Diego Center for Neural Circuits and Behavior, who attempts to better elucidate the long range connectivity of the primary auditory cortex. By using a retrograde tracer cholera toxin B (CTB) that is attached to different fluorescent markers, Lai and co-workers visualize the A1’s organizational structure by tracking and mapping its transmissions. CTB attaches to gangliosides, a lipid in ganglion cells, allowing for the retrograde labeling of neurons. Then, in conscious mice, the researchers utilized two-photon calcium imaging, a technique that tracks fluorescently-dyed calcium ions to monitor the activity of individual neurons in the primary auditory cortex of the conscious mice. The researchers found that the transmissions were rarely sent downstream to more than one unique auditory channel. Instead, the information was transmitted based on the functions of the target area. Understanding the transmission of redundant information in the primary auditory cortex is significant, as it allows for the identification of how extensively the A1 is processing information. Observations of transmission pathways to specific areas of the brain led to the conclusion that functions of the neurons’ distinct targets affect the type of information being sent to them. “Based on the anatomical organization of A1, it is more likely that specific information is being sent downstream …
based on the target’s function,” Lai said. Although an understanding of where and what type of information is being transmitted is crucial, questions regarding the specificity of such information persist and require extensive research.
THE ROLL Nevertheless, winning a game of Roll-A-Ball depends on more than just the ball’s destination. The frequency, intensity, and magnitude of the roll also influence outcomes: the initial outcome of where the ball falls and the final outcome of the game, how much the marker moves. Similarly, multiple factors also affect neural responses and — ultimately — behavior. Sensory processing in the neocortex affects behavior and cognition, making it important to understand the relationship between brain state and sensory responses. Unfortunately, how the brain processes sensory information at the superficial, outer sub-layers of the primary auditory cortex is less understood, even though the majority of intracortical processing occurs here. Complementing Lai’s research on the inner layers of the A1, student co-researchers Elena Westeinde and Kimi Taira of the Isaacson Lab investigated the effects of brain state on sensory responses in the more active second and third layers of the A1. Westeinde and Taira monitored pure tone-evoked responses by using the same method of two-photon calcium imaging on the second and third layers of the primary auditory cortex of mice, in addition to tracking their treadmill activity and the measurement of pupil sizes and sensitivity.
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The strength of a response correlates with the intensity of neural responses to incremental increases in sound frequency, as measured by the peak of fluorescent signals of the recorded neurons. By exposing mice to various sound frequencies and observing the activity in levels two and three of the mices’ A1s, the researchers concluded that at high arousal levels, the range of frequencies that an A1 neuron can process widens, leading to stronger responses to sound frequencies. As arousal levels increase, so does the mice’s sensitivity of the A1 to auditory frequencies, but their A1’s ability to differentiate between frequencies diminishes. In other words, hearing a loud scream at the fair may increase your sensitivity to other sounds, but not necessarily your ability to distinguish between them. Such findings demonstrate that brain state can alter the processing of sensory information in neural circuits. Thus, cognition and behavioral responses are contingent on brain states, supporting the notion that consciousness is not only influenced by our surroundings but also by internal neural activity.
THE AFTEREFFECT Understanding sensory processing enables us to better comprehend the biological process behind forming rational behavioral decisions. However, only a part of the puzzle is complete. We know that a variety of internal factors affect behavioral output. Consider the Roll-A-Ball example. Factors such as eyesight, arm strength, and coordination influence aim and momentum. The marker in roll-a-ball represents the behavior resulting from neural transmissions; this is
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represented by the movement of the ball down the wooden ramp. We can observe how the brain processes multisensory information to output ethologically relevant behaviors. Xiaonan Xing, Vicky Mak, Sachin Sethi, Yinan Xuan, and Jing Wang of the UC San Diego neurobiology department analyzed the mating behavior of Drosophila melanogaster, commonly known as fruit flies, to understand how the different senses connect to construct behavioral outputs. Drosophila males utilize visual, olfactory, tasting, and mechanosensory cues to attract mates because courtship activities include searching, chasing, tapping, licking, and singing at female Drosophila. The student researchers attempted to classify and predict each of these typical mating behaviors through a machine-learning algorithm. By tracking the movements of the flies through video recordings, they observed that the courtship rituals chosen by the Drosophila males were based on the positions and movements of the females. To test their hypothesis, the researchers deprived male fruit flies of their visual capabilities to affect their spatial and temporal perceptions. The researchers also induced genetic mutations to eliminate single sensory cues to determine how certain manipulations affect the courtship strategies of Drosophila males. From observing the ways in which specific sensory information affects behavior essential to the survival of an organism — in this case courtship behaviors for the Drosophila males — scientists can better understand how behavior is influenced by the variety of sensors that process such multisensory information.
CONCLUSION Although the effects of sensory processing on behavioral outputs for complex beings such as humans requires additional research, elucidating the mechanisms behind sensory processing and its behavioral impact on model organisms such as mice and fruit flies facilitates a deeper understanding of the relationship between the two. Additional research into the effects of individual senses on behavior allows us to understand how different types of stimuli influence behavior in unique individuals, including children struggling with spatial processing disorders. Although investigating the details and impacts of sensory processing is similar to Roll-A-Ball, alluring and multi-leveled, this is clearly no game.
The classic Roll-A-Ball fair game directs players to roll a ball up a runway into one of many holes of varying point values. The point value associated with a hole determines how far the score marker moves.
W R IT T E N B Y li a T u Ju V ic k ie K u o & Vickie is a Human Biology major graduating in 2021. Ju lia is a Molecular and Cell Biolog y major graduating in 2022.
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E CANC R T
he average human is made up of around 37 trillion cells. Though different types of cells have different lifespans, billions of them die everyday. Thankfully, the body is equipped with highly regulated processes to ensure that they are replaced with new, healthy cells. Every so often, however, mistakes occur in these processes that lead to one of the most complex group of diseases of the present day–cancer. While cancer may seem like a modern affliction, it was actually first described around 3,600 years ago in an ancient Egyptian medical text known as the Edwin Smith Papyrus. Despite many technological and medical advancements over the millennia and the hundreds of billions of dollars spent in the war against cancer, cancer continues to elude eradication. In spite of the immense complexities, students and researchers at UC San Diego continue to fight in the face of this ever-present threat.
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ONE SIZE FITS SOME what you need to know about cancer & how researchers are fighting back
WHAT DOES “CANCER” REALLY MEAN? One of the greatest misconceptions about cancer is that it is just one disease. “Cancer” is a vague designation for a plethora of illnesses that share one feature in common — the overproliferation of cells. Beyond this feature, every cancer is different. For this reason, what causes a type of cancer in one person may not cause it in another person; what treats cancer in one case may not work in another, even when it is considered to be the same type of cancer. This, in large part, is why cancer is so difficult to fully understand and even harder to cure. Nevertheless, some scientists try to maximize the reach of their work by investigating elements common to multiple forms of cancer. Dr. Dong-Er Zhang, a UC San Diego professor who was recently named a fellow of the prestigious American Association for the
WRIT TEN BY Xave r Audh ya & Andr a Thom as PHOTO BY Mark Jacob ILLUSTRA TIONS BY Cristina Cor ral
Photo: A single 96-well crystal plate out of thousands that test all manners of cellular conditions for a potential immune agonist antibody. Despite the high chance of failure, the prospect of success urges efforts forward.
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Advancement of Science (AAAS), guided Katherine Liu in taking this approach in her research on a protein called RASSF2. RASSF2 is a tumor-suppressing protein, a sort of gatekeeper that ensures everything goes smoothly when new cells divide. When RASSF2 discovers a potentially cancerous situation, it can trigger apoptosis, or programmed cell death. Indeed, without RASSF2 and other tumor-suppressing proteins, cancerous cells can proliferate rapidly, unchecked and unchallenged. RASSF2 activity is repressed in many types of cancer, but little is known about its mechanism. Liu suspects that a particular part of the protein, called the SARAH domain, allows it to be recognized by specific types of E3 ubiquitin ligases, which target the protein for destruction. E3 ubiquitin ligases can do this by modifying the target protein in such a way that it signals another protein, called a proteasome, to come and destroy it. To ascertain whether the SARAH domain contributes to RASSF2 degradation, she created two groups of cells: one where the RASSF2 protein had an intact SARAH domain and another group where the RASSF2 had no SARAH domain, and then subjected them to a wide variety of tests and monitored whether or not the groups responded differently. Not only did she confirm that the SARAH domain was necessary for RASSF2 degradation, but she also identified two specific E3 ubiquitin ligases, PIAS2 and ITCH, that were likely
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responsible for acting on the SARAH domain. While of course there remains much work to be done to further illuminate how these findings will translate across different types of cancer, if PIAS2 and ITCH are indeed vital to RASSF2 degradation, it is possible inhibitors can be designed to antagonize their functions and restore RASSF2’s tumorsuppressing abilities.
FROM ONE TO MANY In another approach, some researchers chose to focus on one type of cancer. At first, this may sound more straightforward, but that assumption is rapidly dispelled after realizing that even one type of cancer may have many subtypes within it. Papillary thyroid cancer (PTC) falls into this category and is becoming one of the most common cancers to exist in the world. There are three primary PTC subtypes; classical, follicular, and tall cell, but little is known about the genomic and transcriptomic characteristics that result in their wide range of prognoses and treatment outcomes. Under the guidance of Dr. Weg Ongkeko, UC San Diego undergraduate student Jaideep Chakladar set out to categorize these characteristics to better discern how these three subtypes different from each other. Chakladar began by determining which immuneassociated (IA) genes were dysregulated in the different PTC variants. While the immune system is known for fighting off infectious pathogens, it also
helps to protect against other things, like cancer. In many types of cancer, the immune system is deregulated, thus allowing the cancer cells to propagate. Chakladar found that these three subtypes share common mutations in several IA genes. This prompted Chakladar to perform computational analyses to better define how each IA gene contributes. He found that depending on the gene, dysregulations were caused both by point mutations and copy number variations. Moreover, he found that the aberrant production of other gene expression regulatory factors, like miRNAs, were also responsible for the abnormal behavior of IA genes. This discovery offers insight into the diverse clinical conditions among subtypes and may even offer insights towards the development of onco-immunotherapies.
DIY: MOUSE MODELS
An E3 ubiquitin ligase recognizes the SARAH domain of RASSF2 and tags it with ubiquitin. A proteasome can then recognize the ubiquitin tag and destroy RASSF2.
A cancer is typically best treated when it is detected early and localized to a particular region. When the cancer metastasizes, or spreads, it is much more difficult to manage. In fact, metastasis is responsible for around 90% of cancer-related deaths. Metastasis occurs when some of the primary tumor cells go through a process called epithelial-mesenchymal transition (EMT), which allows them to become mobile and travel throughout the body. Eventually, they spread to other areas of the body, but in a
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dormant form. When the conditions in that area are “right,” the cancerous cells go through a process called mesenchymal-epithelial transition (MET) and turn back into stationary, active tumor cells, and begin proliferating. In some cases, the traveling cells can remain dormant for years and reactivate years after a patient had been considered free of cancer. Scientists often use animals, such as mice, to study diseases, since animals can better model diseases than cells in Petri dishes. However, no such model currently exists for studying metastasis. This, in part, contributes to a shortcoming in understanding the biological processes that allow metastasis to take place. Dr. Jing Yang mentored Tiffany Lee in establishing a mouse model to study tumor dormancy and metastasis in breast cancer. Lee began creating her model by injecting lentiviruses containing the recombinant gene that codes for the Her2 protein, tagged with a red fluorescent protein (td tomato). When the Her2 protein is overexpressed, it can cause breast cancer. Meanwhile, the red fluorescence allows Lee to track which cells were derived from the initially infected, cancerous cells. She then treated the mice with the antibiotic doxycycline for three weeks to activate Twist1, a protein known to promote EMT and tumor metastasis. Twist1 was tagged with a green fluorescent protein (GFP) so she could
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Lentiviruses can be used to insert the gene for the Her2 protein into mice; this allows a chance for the Her2 protein to be overexpressed, creating a cancer model mouse.
confirm that it was being expressed. From here, she carried out a set of experiments to examine cellular morphology and confirm that stationary (epithelial) tumor cells were transitioning into mesenchymal (mobile) cells due to Twist1 expression. Having established that the tumors were truly metastasizing, she discontinued doxycycline administration in one group to induce MET while continuing it in another to keep the cells in their dormant state. As the lungs are the first area breast tumors metastasize to, she examined them for signs of fluorescence that would indicate what state the cells were in. She found red fluorescent Her2 in the discontinued treatment group, indicating that the cells had exited their dormant state and begun metastatic growth. In the continued treatment group she found green fluorescent Twist1, indicating that cells had migrated and were still in their dormant state. Experiments like Lee’s are extremely complex — she’s required to take all factors into account for each experiment that’s conducted to ensure her observations are real. Her work in establishing this model will be further expanded upon in the future and may play a vital role in further investigating the molecular mechanisms of cancer metastasis, and hopefully finding better treatments.
CONCLUSION The American Cancer Society estimates that almost 1 out of every 3 people will develop some type of cancer over their lifetime. It is unquestionably one of the most prevalent and complicated diseases we face today. Despite the enormous diversity and extreme complexities, student researchers at UC San Diego like Katherine Liu, Jaideep Chakladar, and Tiffany Lee are helping to pave the way for a better understanding, and bring us closer to finding a definitive and lasting cure.
WRITT EN BY Xaver Audhy a & Andra Thoma s Xaver is a bioche mistry & Cell Biology major gra duating in 2019. Andra is a Huma n Biology major graduating in 20 21.
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MAINTAINING the bridge TO THE BRAIN
how researchers at UC San Diego are finding new methods to combat neurodegenerative diseases
magine a world where both neglecting a problem and trying to fix it pose an equally high risk of damage. Welcome to the world of our brains, their neurons, and the diseases that may be inflicted upon them. Neurodegenerative diseases are the unfortunate repercussions of erroneous genetic and physiological interactions, and are caused by factors that are often not yet fully understood by science. They can arise due to the neglected degradation of neural cells (as in the case of Huntington’s), or due to an attempt at fixing an issue which could result in a disorganized immune response and eventually neural cells destruction (as in Amyotrophic Lateral Sclerosis). With a vast range of implications, neurodegenerative diseases block neural access to key regions of the brain and hinder their function, thereby making it difficult for individuals to keep to their daily routine.
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As a result of increased life expectancies, more and more people are experiencing the effects of these diseases. It has become imperative to monitor the progression of these diseases, understand the mechanisms through which they propagate, and ultimately find cures to prevent them in the future. Fundamentally, this entire process is similar to taking care of a crying child — you can only make them feel better if you succeed in identifying the cause of their discomfort, assessing the severity, and then sketching a plan of action to eliminate the issue.
DIAGNOSIS: OBSERVING KEY FEATURES OF MSA A common feature of many neurodegenerative diseases is that they can be difficult to diagnose early on. One such disease known as Multiple Systems Atrophy (MSA), is characterized by tremors and loss of coordination and impairment of many autonomic body functions, such as regulation of blood pressure, body
W R IT T E N B Y sh a D ev av ar ap u A hs an U sm an i & T vi PH OT O BY Michael Endow & Anne Mari e Berry IL LU ST RA TI ON S BY Vicky Hoznek sqonline.ucsd.edu•• 27 27 sqonline.ucsd.edu
temperature, and breathing. What’s more, diagnosing MSA is still extremely challenging in spite of these severe symptoms. But this did not deter undergraduate student Jessica Kim. Under the supervision of graduate student Jennifer Mott and Dr. Paula Desplats at the Department of Neuroscience and Pathology, Kim hopes to combat MSA by finding new ways to diagnose the disease. The focus of their research was to characterize microRNA (miRNA) levels in MSA. An miRNA is a noncoding sequence of RNA that serves as a regulatory switch for gene expression. Any gene in our DNA that is going to be expressed first needs to be transcribed into a strand of mRNA. This strand of mRNA can then be translated into a protein which will carry out physiological functions, as posited by the central dogma of molecular biology. As a part of this process, miRNA fine tunes gene expression by silencing, or turning off, certain harmful genes encoded in the newly transcribed RNA. By examining miRNA levels, the researchers could understand how MSA progression corresponds to gene expression. This method for monitoring disease progression can be likened to the quality control of many regulatory agencies. For example, if the FDA were to fail in performing a quality check on lettuce being used, there is a chance that some percentage of salads made may have contaminated lettuce. Salads with contaminated lettuce would thus be unsafe for human consumption, posing a health hazard for the consumers. In the same vein, when looking at frozen brain tissue, the team found that miRNA expression had been altered
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and deregulated, such that certain genes were not being turned off as they should have been. By assessing miRNA levels, the researchers can narrow down neural pathways that could be affected as MSA progresses. Furthermore, their research demonstrates how monitoring indicators as far down as even the molecular level, such as miRNA levels, can serve as a powerful diagnostic tool in tracking neurodegenerative disease progression.
ANALYSIS: A LOOK INTO ALS PROGRESSION While tracking disease progression is an important step forward, it is also important to understand how a disease induces damage in order to design effective therapies. In their research, recent UC San Diego graduate Joshua Asiaban and other members at the Cleveland Lab at UC San Diego attempted to gain a better understanding of the mechanisms of progression behind Amyotrophic Lateral Sclerosis (ALS), another rare neurodegenerative disease. What makes understanding ALS so urgent is its rapid progression in patients. Those diagnosed with the disease often pass away within 4 years, often because they lose the ability to breathe on their own. This is primarily due to fibrotic scarring, a phenomenon in which attempted repairs of neuronal connections results in stiffened, scarred tissue. This stiffened tissue prevents axons—the branching tail-ends of nerves—from forming junctions with other neurons. Think of fibrotic scarring as akin to repair efforts on a highway. In attempting to repair damaged pavement,
an entire section of the highway has to be closed down, and as a result, connection could be lost between two cities. In our case, however, fibrotic scarring instead means a loss of connection between our brain and body. For those with ALS, this loss manifests as muscle twitching and weakness that makes tasks such as speaking, eating, and even breathing difficult. To clearly observe progression of ALS, the team first created an isolated model of the disease using microfluidic chambers (pictured) to visualize how ALS-causing proteins contributed to fibrotic scarring. They set up a chamber to grow motor neurons which they would then damage in order to observe the effects ALScausing proteins would have on recovery. What they found using this setup was that ALS-causing proteins would suppress axonal regeneration, meaning that the damaged ends of these neurons couldn’t be repaired anew. This is a crucial finding because if the motor neurons lack the ability to regenerate their axons they lose their ability to signal with muscles and other neurons, thus providing a valuable insight into how ALS results in irreparable damage to neurons. Two connected microfluidic chambers with motor neurons and muscle cells are used to study signalling patterns from neurons to muscles. Simulating conditions as present in ALS enable researchers to visualize the loss of connection between the two compartments over time.
However, the team didn’t stop there. In addition to demonstrating the applications of microfluidic chambers as a valuable tool in observing disease progression, they also showed how this tool can be used to provide a clear environment
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to test treatments. The team then utilized a system of two connected chambers, which grew either motor neurons or muscle cells, in order to model signaling by neurons to the muscles. This setup allowed the researchers to visualize the loss of connection between the two compartments over time, simulating the conditions for many neurodegenerative diseases like ALS. Moreover, the set-up also allowed for testing of treatments which could promote reconnection or prevent disconnection. Moving forward, continued use of these microfluidic chamber cultures could prove to be a valuable tool in understanding the progression of many different neurodegenerative diseases and developing new treatments for these diseases.
PREVENTION: FINDING WAYS TO INHIBIT THE SPREAD OF HUNTINGTON’S DISEASE After identifying the molecular dynamics of a disease, the next step is determining a plan of action for curbing the damage being done to the brain as a result of the disease. This fight to find treatments is evident through Zeljana Babic, whose work at the Brady Lab seeks to identify a novel approach to identifying the neuroprotective effects of a protein called TRiC Chaperonin in treating Huntington’s Disease. Fundamentally, Huntington’s Disease, like other neurodegenerative diseases, such as Alzheimer’s, Parkinson’s, and ALS, can be attributed to the accumulation of misfolded proteins which ultimately result in abnormal muscular motions and cognitive impairments. Think of donuts on a production line that begins to malfunction. Due to a certain segment of
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the line functioning incorrectly, the donuts begin to get formed in a distorted shape; the longer the line runs, the more distorted donuts are produced. Similarly, in Huntington’s, a trinucleotide sequence composed of the DNA bases C, A, and G occurs repeatedly within the HTT gene, which ultimately codes for huntingtin protein (Myers, 2004). Accumulation of CAG repeats crowd the protein, distorting its intramolecular interactions and thereby leading to misfolded HTT. The interactions a protein can engage in, the bonds it can form, and most importantly, the functions it possesses are all defined by the proteins’ structure. This is why the malformation of a protein could potentially lead to disease. Indeed mutant HTT (mHTT) is a defining characteristic in HD and has been shown to lead to a substantial loss of a certain class of neurons known as medium spiny neurons (MSNs). The pathways of these MSNs are disrupted and degenerated by the mHTT, resulting in atrophy, or death, of the MSNs. These MSNs coordinate information regarding motion from cortical, thalamic, and brain stem inputs, which explains why Huntington’s Disease leads to movement abnormality and cognitive issues. Once the problem is identified, the intervention kicks in, and this is what has been studied and implemented in the Brady Lab. Zeljana Babic and her team sought to treat axonal dysfunction and cortical atrophy under the hypothesis that TRiC chaperonins could reduce activity of mutant huntingtin protein. Chaperonins are proteins that provide favorable conditions for the correct folding of other proteins, thus preventing aggregation. Babic and her team hypothesized that the
Due to mutation, normal huntingtin proteins lose their function, which leads to a loss of medium spiny neurons (MSNs). The disruption of these neurons’ pathways prevents their function of coordinating information, ultimately causing abnormality in movement, and cognitive impairments.
effects of mutant HTT could be mitigated through action of the chaperonin; therefore, in their research they targeted the mutant, misfolded protein with chaperonincontaining elements that promoted corrected protein folding in order to prevent the damages associated with Huntington’s disease. What they found was precisely that: a viable route to preventing atrophy progression using chaperonins, as opposed to allowing damage to the MSNs to slowly build up over time.
Together, all of this research shows that, in order to address neurodegenerative disease, we must look for viable routes towards identification, analysis, and finally prevention before the disease can greatly damage the brain. Considering how prevalent these diseases are becoming in our population and how devastating they can be, it’s only becoming more important that we focus on preventing and ultimately even treating these diseases. Going forward, it’s also important to understand that research into neurodegenerative disease as being about more than just seeking cures. Rather, we are attempting to build back the bridge between the brain and body, and in doing so are giving those afflicted their bodies back.
W R IT T E N B Y Ahsan Usmani & pu T v is h a D e v a v a ra Ahsan is a G eneral Biolog y major graduating in 2020. Tvish a is a Human Biology majo r graduating in 2022.
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2018 UNDERGRADUATE BIOLOGICAL SCIENCES STUDENT RESEARCH SHOWCASE
RESEARCH
POSTER W
Generating the First Inducible Mouse Model for the Study of Sturge-Weber Syndrome MONICA ACOSTA DR. J. SILVIO GUTKIND PIRC-NET: Twitter-based on Demand Public Health Framework for HIV Risk Estimation SAMARTH AGGARWAL DR. NADIR WEIBEL
Medial Entorhinal Cortex Inputs are not Required for CA3 Cells to Retain Trajectory Information in a Spatial Memory Task VINEETH VARMA ALLURI DR. STEFAN LEUTGEB Benefits of Microfluidic Chambers for Neuroscience Research JOSHUA NISAN ASIABAN CLEVELAND LAB
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INNERS
ROCIO BARAHONA ANDREA KLEIN RICHARD NIEDERECKER KYLE SANCHEZ KIMI TAIRA & ELENA WESTEIND
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Generation of an LRP6 Deficient Cell Line via CRISPR-Cas9 ROCIO ALEJANDRA BARAHONA DR. KARL WILLERT Analysis of Isolated Streptomyces Strains though Bacteriophage Host Range Experiments and 16s rRNA Sequencing MAYA ELIZABETH AMBROZIAK DR. SWARNA MOHAN Platelet-mediated Innate Immunity Against B. Anthracis MAYMYINTTHANDA KYAW DR. VICTOR NIZET
Cellular Mechanisms of Neuroprotective Effects of TRiC Chaperonin in Huntington’s Disease ZELJANA BABIC DR. CHENGBIAO WU
Cardiac Fibroblast (CF) Activation Under High Glucose Treatment and its Implications for Fibrosis MADONNA ASHRAF KONDOS HAFEZ DR. OMENS AND DR. VILLARREAL
Comprehensive Genomic and Transcriptomic Analysis of Papillary Thyroid Carcinoma Reveals Common and Unique Mutations and Immune-associated Gene Expression Dysregulations Among the Various Cancer Subtypes JAIDEEP CHAKLADAR DR. WEG ONGKEKO
Determining the Developmental Stages that Require Nascent Protein Polypeptide-Associated Complex -Alpha (NACA) for Drosophila Heart Development PRACHI ANSHU DR. ROLF BODMER
Antibiotics in your Backyard ANDREA BIJU DR. SWARNA MOHAN Cracking Open the Black Box of Neural networks ARKIN GUPTA DR. GABRIEL A. SILVA Fibrotic Scarring in Neurological Disorders EZEKIEL ANTHONY HAENELT DR. RICHARD DANEMAN Combining Stiffness and Stretch to Study Cardiac Fibroblast Pro-fibrotic Activity GEORGE KENZO GILLES DR. ANDREW MCCULLOCH In Search of Novel Antibiotic Therapeutics LAUREN ALEXA BRUMAGE DR. JOE POGLIANO
The Parasitic Plant Dodder (Cuscuta Californica) Infection of Buckwheat (Eriogonum fasciculatum) is Higher in Wetter Soils ANTONIA KELETSO BOCK DR. ELSA CLELAND IL-6 Activated STAT3 Promotes Oxidative Metabolism in Obesity JULIA HELEN DELUCA DR. SHANNON REILLY A Comparison of Anxiety, Depression, and Stress Mood Scores in Breastfeeding Women Who Use Marijuana to Those Who Do Not Use Marijuana SAMANTHA LEE BOCCIA DR. KERRI BERTRAND Ligand-dependent Regulation of 3D Chromosomal Architecture and Subnuclear Structures YEEUN KIM DR. MICHAEL GEOFF ROSENFELD
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The Expression of DRA Following Enteric Infection ANDREW QUACH DR. SOUMITA DAS Improved RNA-hairpin Recognition in the RNA-TAG System DYLAN WALKER MILLS DR. NEAL DEVARAJ Using Social Network Analysis to Measure Student Interactions and Dynamics in Group Work JOSHUA PEI LE DR. STANLEY LO Rat Decision Making in Weighing Quality Against Quantity when Evaluating Rewards GRACE LO DR. PAMELA REINAGEL Determining the Role of Candidate Wound Signature Molecules in Activation of γδT Cells Using CRISPR/Cas9 GENEVRA ERIN MAGLIOCCO DR. WENDY HAVRAN Characterizing Wnt16 Signaling with Noncanonical Wnt Reporter Assays HANNAH ELISABETH MORRIS LITTLE DR. KARL WILLERT Improving Cyanobacteria Strain Fitness in Outdoor Ponds JIAYAN TAN DR. SUSAN GOLDEN
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What Strategies Do Students Use on Free Response Test Questions? MATTHEW ARASH NEDJAT-HAIEM DR. JAMES E. COOKE YAP and MRTF-A, Transcriptional Co-activators of RhoAmediated Gene Expression, are Critical for Glioblastoma Tumorigenicity ANDREA LAUREN KLEIN DR. JOAN HELLER BROWN Wnt-Fzd Specificity in Hematopoietic Stem Cell Development JORDAN ALI SETAYESH DR. KARL WILLERT Development of Protein Loaded Hydrogels for Delivery to Peripheral Nerve RICHARD WOLFGANG NIEDERECKER DR. YANG Understanding the T Cell Receptor (TCR) Architecture Using a Membrane Reconstitution System SANDRA KHALIL RABAT DR. ENFU HUI Identification of New Antibiotics with Cell Wall-targeting and Anti-cancer Mechanisms JASON FAIRBANK NIDEFFER DR. JOE POGLIANO
Isolation and Characterization of Bacteriophage from Soil LINDA VU DR. SWARNA MOHAN Genomic and Proteomic Analysis of the Novel Streptomyces Phage Darolandstone SAISRI RAVI DR. SWARNA MOHAN A Global Transcriptional Network Connecting Noncoding Mutations to Changes in Tumor Gene Expression KYLE SALINAS SANCHEZ DR. TREY IDEKER Evaluating Clinical Texts Using Natural Language Processing to Predict Patient Neurological Disorders JIGAR PATEL DR. CUN-NAN HSU DR. JULIAN MCAULEY DR. NDAPA NAKASHOLE DR. ERIK VIIRRE “What’s in an Argument?” Using a Simplified Toulmin Framework to Quantify Student Arguments ANH THI HOANG TRAN DR. LISA MCDONNELL Brain State-dependent Modulation of Sensory Representations in Layer 2/3 of Primary Auditory Cortex ELENA ADRIENNE WESTEINDE DR. JEFF ISAACSON
Generating Substrates of The Ubiquitin Proteasome System with Optics YOUSIF IMAD SLAIWA DR. RANDY HAMPTON Understanding Students’ Knowledge Frameworks about Biology Research JAKE JAMES S SY DR. LISA MCDONNELL Engineering Entry Inhibitors to More Potently Bind HIV Envelope Proteins AARON HOANG KHANG TRANDO DR. WILLIAM SCHIEF Exploring the Role of Sensory Information in Patterning Complex Social Behaviors in Male Drosophila Melanogaster using a High-Resolution Assay XIAONAN XING DR. JING W. WANG Probing the Descending Pain Pathway CONNOR EVAN WEISS DR. MATTHEW BANGHART Plagiarism Awareness Writing Assignments Reduce Plagiarism and Writing Problems in an Upper Division Laboratory Course ANQI YANG DR. LISA MCDONNELL
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Discovery and Application of the RNA-Targeting CRISPR Effector Cas13d in Transcriptome Engineering ELEANOR WANG DR. PATRICK DAVID HSU
Smooth Muscle Cell Heparan Sulfate Proteoglycans Mitigate Atherosclerosis Formation VINEET TUMMALA DR. PHILIP GORDTS
The ELMO1, A Microbial Sensor Regulates Bacterial Clearance and Endo-Lysomal Signaling FATIMA FAKHIR USMANI DR. SOUMITA DAS
Genome Analysis of Streptomyces Phage Hank144 ALEXANDRA CECILIA WESTGAARD DR. SWARNA MOHAN
HONORS RESEARCH
P O S T E R W IN
Ezh2 Loss is Associated With Aberrant Chromatin Structure in Progenitor and Mature Mouse Neutrophils ARMON ENAYAT AZIZI DR. RAFAEL BEJAR Studying the Role of Protocadherin Genes in Regulation of Human Neuronal Morphology In Vitro YALIN DENG DR. FRED GAGE
The After-Antibiotics Study: Investigating the Implications of Antibiotic Treatment for Urinary Tract Infection on the Urinary Microbiome and Metabolome in Young Women ANIKA NAWAR ULLAH DR. ROB KNIGHT
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NERS SEAN GUY ZHIJIAN LI
Mutation Rate Variation within the Yeast Genome SEAN EDWARD GOMEZ GUY DR. SERGEY KRYAZHIMSKIY What is the Role of PDLIM1 in Oxygen-Induced Retinopathy? JOSEPH PATRICK MILLER DR. RICHARD DANEMAN Deregulation of miRNA Profiles in MSA May Alter Oligodendrocyte Maturation Pathway and Contribute to α-syn Accumulation TAEYEON KIM DR. PAULA DESPLATS
Spatial Organization and Functional Characterization of Auditory Cortex Projection Neurons MANDY LAI DR. JEFFRY ISAACSON
The Recruitment of TRF2 to TATA-less Promoters via Transcription Factor Interactions JACQUELYN TRUONG DR. JAMES KADONAGA
Characterizing Non-catalytic Domains of Unconventional Deadenylase TOE1 and Investigating Their Biological Importance on snRNA Processing ZHIJIAN LI DR. JENS, LYKKE-ANDERSEN
Circuit and Behavioral Investigation via Optogenetic Manipulation in Target-Cell-Type-Defined Corticostriatal Pathways MARCUS LAWRENCE TURNER DR. TAKAKI KOMIYAMA
Investigating the Role of Endogenous Opioids in Learning and Motivation JOSE ANDRES MENDOZA LOPEZ DR. MATTHEW BANGHART
Measuring Rat Impulsivity and Cognition using Delay Discounting and Visual Attentional Engagement Tasks VISHAL VENKATRAMAN DR. PAMELA REINAGEL
Inhibition of D1R Expressing Neurons in the Dorsal Striatum Promotes Meth Addiction-like Behavior KHUSH MEHUL KHARIDIA DR. CHITRA MANDYAM
Investigating the Role of Zeb2 Transcription Factor in CD8+ Memory T cell Differentiation and Homeostasis TOMOMI MARIE YOSHIDA DR. ANANDA GOLDRATH
Defective Mechanism of Nerve Growth Factor Secretion in the Context of HSAN Type V XAVIER MINH MATHIEU ORAIN DR. CHENGBIAO WU
Oxidative Stress is a Cause of Reduced Fitness in Copepod Hybrids PASSENT ASHRAF AMIN YOUSSEF DR. RONALD BURTON
Uncovering the Secret Life of Genes CAROLINA GONZALEZ BRAVO DR. GALIA DEBELOUCHINA
Loss of RIAM in B Cell Impairs T-independent Immune Response YUYA ZHAO DR. JOSEPH CANTOR
A Maize CCAAT Box Binding Transcription Factor that Regulates Defense Against Fusarium Venenatum ANH-DAO LE TONG DR. STEVEN P. BRIGGS
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MASTERS RESEARCH
WI POSTER
A Mechanistic Understanding of the Elusive Black Eschars in Cutaneous Anthrax JAMMAL KHALED ABU-KHAZNEH DR. ETHAN BIER Novel Approach to Investigate the Role of Human Milk Oligosaccharides on Neglected Infectious Diseases SHAMS A AL-AZZAM DR. LARS BODE
NNERS
TIFFANY LEE EMMA WU
Nicotine-induced Neurotransmitter Plasticity in the Substantia Nigra I-CHI LAI DR. DAVIDE DULCIS
Circadian Regulation of Defense Responses via NPR1 Expression in Arabidopsis CIARA ALEJANDRA ALVAREZ-MALO DR. JOSE PRUNEDA-PAZ
Observing Horizontal Gene Transfer of iRon Update Siderophore Transport Island (RUSTI) in Native Cheese Bacteria and Creating a Better Understanding RUSTI’s Role in Species Specific Growth in the Cheese Microbial Community GILLIAN TORREY BELK DR. RACHEL DUTTON
Building on Bloom’s: Understanding the Structure of Bloom’s Revised Taxonomy in Biology BIANCA HANAKO ENDO DR. STANLEY LO
Establishing Twist1-Inducible Breast Cancer Mouse Model to Investigate Tumor Dormancy and Metastasis TIFFANY LEE DR. JING YANG
Quantification and Epigenetic Analysis of Brain-Derived Neurotrophic Factor in Huntington’s Disease ASHLEY MICHELLE GUTIERREZ DR. JODY COREY-BLOOM
Stress Signaling Regulates Mating Decision in Saccharomyces Cerevisiae YUTIAN LI DR. NAN HAO
Salivary Huntingtin Protein Levels are Elevated in Huntington’s Disease Patients AMEERA SAMAHER HAQUE DR. JODY COREY-BLOOM MD, PHD
Identification of SARAH Domain-Specific E3 Ligases Targeting RASSF2 for Degradation TIN HENG KATHERINE LIU DR. DONG-ER ZHANG
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Investigating the Role of the Adult Maize Leaf Cuticle in Providing Pathogen Resistance ALBERT MINH TRI NGUYEN DR. LAURIE SMITH Circadian Entrainment of Bipolar Patient Fibroblasts VICTORIA SHANNON NUDELL DR. MICHAEL J MCCARTHY Auditory Discrimination Learning in a Rodent Model of Human Targeted Cognitive Training BENJAMIN ZALMAN ROBERTS DR. JARED YOUNG Expression of VGLUT2 is Upregulated After Injury to Dopaminergic Neurons in Mouse Substantia Nigra Pars Compacta XINYI SHEN DR. TOM HNASKO Molecular and Behavioral Characteristics of Epileptogenesis in a Rat Model of Medial Temporal Lobe Epilepsy GABRIELLE JESSICA MADERA SUAREZ DR. JILL K. LEUTGEB
Caspase-4 and -5 Mediate Non-canonical NLRP3 Inflammasome Activation to Induce Interleukin-1β in Human Primary Macrophages Exposed to Human Immunodeficiency Virus Type-1 GU-rich Single ssRNA RACHEL KIM-CHIE TO DR. STEPHEN SPECTOR Potential Mechanisms of the Influence of Cholesterol on Pathogenic Amyloid Precursor Protein Processing LOUIE WANG DR. LAWRENCE S.B. GOLDSTEIN Using the CRISPR/Cas9 System and Human Isogenic Neurons to Elucidate the Genotype-Phenotype Relationship of Niemann Pick Type C1 EMMA YATING WU DR. LAWRENCE GOLDSTEIN Modulation of Aberrant Neural Circuit Activity by Neuropeptides in the C. Elegans Locomotor Circuitz KINGSTON ZHOU DR. YISHI JIN
Dual Overexpression of SIRT1 and Knockout of GCN5 in Adult Skeletal Muscle Does Not Alter Exercise Capacity or Mitochondrial Function in Mice SHAHRIAR TAHVILIAN DR. SIMON SCHENK
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Under the Scope
Division of Biological Sciences University of California, San Diego sqonline.ucsd.edu