Under the Scope is the product of nearly a year’s worth of meticulous investigation and effort by student writers, editors, illustrators, photographers, and designers. We welcome you to join us in celebrating the power of student research in the UC San Diego community through this union of scientific discovery and communication!
For the first time since 2019, UC San Diego’s School of Biological Sciences held their annual research showcase in collaboration with Saltman Quarterly. Undergraduates, honors thesis students, and masters students presented their research to peers and faculty judges. Inspired by the display, our Under the Scope writers delved into the variety of biological topics presented and selected two research studies with overlapping topics that piqued their curiosities. Each resulting article focuses on student research in two laboratories exploring similar themes. Through interviews and countless draft revisions, these writers challenged their personal knowledge and developed their writing skills as they crafted these articles.
Our publication begins by delving into the cellular processes behind organismal development, focusing on microtubules and cell contractility. The next article presents current cancer research to understand what happens when cell division goes wrong, in the hopes of identifying anti-cancer drug targets. We then shift to the central nervous system, looking at how to protect the spine in both embryonic development and neuron regeneration. Stepping away from humans and turning to songbirds and honeybees, the next article studies unique animal communica-
tion methods involving song and dance. Our final article explores how the brain transforms during addiction and relapse using rats as an experimental model. If you are interested in discovering more research conducted by students on campus, our publication ends with a full list of participants and poster titles for the 2023 Biological Research Showcase.
The diversity in research topics demonstrates not only the boundless curiosity of UC San Diego student researchers, but also the opportunities within biological research to understand a variety of life’s biggest mysteries. From mitigating disease to discovering the language of various species, student researchers continue to make vital contributions to scientific knowledge. In sharing these discoveries, we commend the efforts and curiosities that students pursue as they begin their scientific journeys.
Without further ado, we are proud to present Volume 14 of Under the Scope.
Amoolya Chandrabhatta and Emily White Editors-in-Chief, Saltman Quarterly 20232024
When we think of developmental biology, what comes to mind? Developmental biology, a constantly evolving field of study, largely focuses on processes involved in the reproduction, maturation, and differentiation of cells. Previous work in the field has generated a complex understanding of cellular division and replication. Now, fascinating cellular components are revealing more of what drives development. At UC San Diego, the Jin and Oegema/Desai Labs explore microtubules and cell contraction in cellular division, and how they impact model organism Caenorhabditiselegans’ability to reproduce and survive the embryonic stage. These labs are exploring how mutations affect these cellular components and therefore impact an embryo’s ability to develop properly.
Microtubules and Temperature Sensitive C.elegans
At the Jin Lab, graduate researcher Kancheng Yin works with the Caenorhabditis elegans (C.elegans) model, or roundworm, to identify the effects of genetic variations on the development of the C.elegans in different temperature conditions. The genetic variations that they identified impact the tubulin proteins making up chains of microtubules within the cells of living organisms. Microtubules play an essential role in cell morphology as well as transporting cargo. Despite the importance of microtubules, there is more to be discovered about their ability to influence physical phenotypes such as temperature sensitivity. While wild type C. elegansdevelop and reproduce normally in 15-25ºC, the temperature sensitive phenotype resulted in C.elegans producing smaller and fewer offspring at 20ºC, and no progenies at all at 25ºC. Within this experiment, Yin works on identifying and mapping the genetic regulators for microtubule synthesis that result in this observed effect on C.elegans development.
Yin used a technique known as forward genetic screening, a method of discovering the genetic cause for a particular observed trait, to determine the mutation causing temperature sensitivity in C.elegans . This procedure first involved mutagenizing the model organism through the use of chemicals or radiation to purposely induce random genetic mutation. In this case, the Jin Lab utilized a chemical known for inducing single nucleotide base pair changes in the DNA sequence. Within the highly mutated worms, the researchers identified worms displaying the temperature sensitivity phenotype and proceeded with the screen by mating the EMS-treated mutated worms of interest with each other to make offspring referred to as the F1 generation. This F1 generation was then crossed with the wild type, unmutated worms to produce an F2 generation with a further diluted list of mutations to examine. From there, researchers examined the genomes of worms involved in the crosses and worked backwards to determine
Cell Division
A cell undergoes cytokinesis in order to divide into two new daughter cells. An even cleavage site allows for symmetric division of the cells.
the specific mutation negatively impacting the development of C. elegansembryos under higher temperatures.
How did researchers determine the genetic cause of this particular conditional development? The researchers compared the genomes of previous generations in order to determine the single nucleotide mutations associated with the temperature sensitive phenotype. By comparing roughly 300 single nucleotide polymorphisms found in the genomes of the worms, the lab determined the gain-of-function mutation resulting in a single change in the amino acid sequence of the gene encoding alpha tubulin-1 (TBA-1),
one of the alpha-tubulin proteins making up microtubules.
TBA-1 is in a class of proteins responsible for forming polymer chains that serve as microtubules in our cells. While multiple alpha-tubulin proteins serve the same purpose, their genetic sequences vary. Additionally, only a single base-pair change changing a single nucleotide causes this vastly different phenotype. Altogether, this discovery introduces interesting prospects for research regarding the unknown effects of microtubules, and how mutations within them can affect progeny viability, with other potential effects on development.
the opposing cell poles. This difference in pressure allows the cell to split at the equatorial band.
Cell Contractility and Embryonic C.elegans Development
In addition to microtubules, organism growth also depends on cell division. At the Oegema/Desai Labs, postdoctoral researcher Dr. Aleesa Schlientz investigates the effect of contractile pressure on cell division in C.elegans . Contractility functions like cables on a suspension bridge by using tension; cables contract when pulled together and relax when pulled away. Contraction of cell surfaces can change the shapes of cells and ultimately tissues,
and it also helps to cleave one cell into two during the end of cell division (cytokinesis). In the cellular environment, actin (a cytoskeleton protein) functions similarly to bridge cables, and myosin applies force to them.
Schlientz uses C.elegansas a model system for these contractility studies because she finds their contractile machinery to be highly similar to that of human cells. In both humans and worms, contractile movement operates based on regions of high and low contractility. The vertical “equatorial” band in the middle of a dividing cell employs high contractility, and the poles on each opposing end of the cell experience low levels of contractile pressure. This balance allows the cell to produce a symmetric cleavage site, and eventually two daughter cells with all organelles. But what causes these differences in cellular contraction? Schlientz researches the signaling that may create different levels of contraction in order to understand what confers a normal cytokinesis and embryonic development for C.elegans . The ability to correctly divide is vital
for successful embryos, since chromosomal distribution depends on cytokinesis.
One type of signaling Schlientz works with involves the protein Cyk4, which helps activate chemical signals that tell the cell to contract at the equatorial region and split in two. To study this process, she injects wildtype parent worms with a mixture of plasmids. Some plasmids will create a break in the genome, and others contain a newly engineered “transgene” that codes for an altered Cyk4. This transgene integrates into the worm genome at the site of the break. After verifying that the offspring inherited this transgene, she injects the worm progenies with engineered double-stranded RNA (dsRNA) that becomes cut by enzymes in the cell. Cellular machinery then removes any of the original gene’s messenger RNA (mRNA) that matches this foreign dsRNA. Essentially, the transgene replaces the original gene that was disabled by a corresponding dsRNA. The embryo expresses only the engineered transgene, which affects its cellular development thereafter.
sent for whole genome sequencing
used for genetic mapping
F2:
original line (mutated with EMS)
wild type less mutated F1 generation
1 color = 1 mutation
wild type
For Cyk4, Schlientz edits the transgene to produce new variations of residues on the protein. By changing the protein structure, she can see how the transgene affects signaling. She monitors the embryo’s phenotype at the site of
to the cell cortex, producing tension in the membrane. She’s discovered that other proteins associated with Cyk4 have the unusual ability to turn signal activators both off and on– conveying just how intricate this process can be. expresses phenotype expresses phenotype doesn’t express phenotype doesn’t express phenotype
contractility by watching multiple rounds of embryonic cell division under a microscope. Ultimately, either the transgene can lead to two healthy daughter cells that experience wild-type contractility, or it will lead to one big cell that does
not divide—a nonviable embryo. This end result indicates how a certain Cyk4 structure impacts cellular contraction. Holistically, she’s investigating the molecular details of how signals directing contraction get from microtubules
Significance of Research and Future Directions
Both the Jin and Oegama/Desai Labs are bringing new points of interest into the intersection between the fields of developmental and cellular biology.
As a lab focused primarily on neurobiology, the Jin Lab hopes to use this research to investigate how microtubules are involved in maintaining the shape and function of the neuronal axon over time. In particular, since Alzheimer’s Disease results in the breakdown of microtubules, this research opens up discussion on whether the destruction of microtubules is a causative effect in the onset of the disease.
At the Oegema/Desai Labs, understanding the signaling that
occurs during cell division allows for further exploration of intracellular communication. During cytokinesis, different cellular parts (like spindles and the cortex) “talk” to each other using signals. By understanding signaling between different cellular components, we can learn more about how all cells operate.
Between the microtubules studied by the Jin Lab and the cell contraction studied at the Oegema/ Desai Labs, both research teams are making discoveries regarding the forces behind cell and organism development. By continuing investigations into the cellular machinery driving growth and division, we can fully understand the journey from embryo to organism.
MatingprocessbetweentheoriginalEMStreatedandwildtypeC.elegansyieldsanF1 generation. The F1 C. elegans then mates again with a wild type to produce offspring that were examined in order to determine the single point mutation responsible for the temperature sensitivity phenotype.
Hijacked: How Cancer Comes to Life
written by MEGHANA HARIPRASAD PLOY TECHAWATANASUK
illustrated by AMBER URENA
photographed by INAYA NICHOLLS
What happens if one day your cells start growing at a faster pace? You might tire faster on your morning run, notice a drop in the numbers on the weight scale, or even observe a bump that was not there before—a tumor. These common symptoms of cancer indicate the transformation of normal cells to cancerous cells, but how does this process occur? At UC San Diego’s Moores Cancer Center, the Gutkind and Chen Labs study the regulation of mitosis in cancer cells, furthering our understanding of how normal cells turn cancerous.
“A normal cell experiences uncontrolled proliferation”
In a normal cell, mitosis is the process of cell division in which a cell replicates its genetic information and splits into two identical daughter cells, allowing for organismal growth. Chemical signals from other cells and the environment initiate the process of cell division, however, mistakes can occur. For example, key proteins involved in regulatory processes of mitosis can accumulate mutations, increasing the risk of uncontrollable cell growth. Mutations are any change to an organism’s DNA sequence during DNA replication and cell division, occurring spontaneously or from exposure to carcinogens and other environmental factors. Over time, mutations accumulated in expressed regions of a gene can change protein function, which may be associated with disease traits, such as sickle-cell anemia or cystic fibrosis.
For a normal cell to undergo oncogenesis, or transform into a cancer cell, mutations must accumulate in two types of genes: tumor suppressor genes and protooncogenes. Tumor suppressors are responsible for slowing down the
progression of the cell cycle. In a normal cell, they act like brake pedals on a car, coding for proteins that signal the cell to stop dividing and undergo cell death if something is wrong. Mutations that damage this regulatory mechanism may inactivate functions or reduce expression of tumor-suppressor genes. However, mutations in only tumor-suppressor genes are insufficient for cells to turn cancerous; mutations must also occur in proto-oncogenes. Normally, proto-oncogenes code for proteins responsible for cell proliferation but are inactivated in the cell once the processes they regulate are completed. With the accumulation of mutations, proto-oncogenes act like a gas pedal constantly being pressed, permanently activating the proteins and causing the cells to incessantly divide. With mutated tumor suppressor genes and protooncogenes, a normal cell experiences uncontrolled proliferation in a localized region of the body and eventually spread of invasive growth, or metastasis, becoming a cancer cell.
Plasma Membrane GPCR
Oncethe ligand binds at theGPCR in the plasma membrane,theG-protein interactioninitiatesaphosphorylation cascadethroughmultiplekinases, includingFocalAdhesionKinase (FAK),adruggabletargetinvolvedin cellproliferationandthereforeuveal melanoma.
FAK inhibits HIPPO Pathway, which usually represses YAP1 expression, therefore dominating YAP1 representation
FAK activates YAP1 directly
GPCRs: External Stimuli and the Kinase Cascade
Mutations in other regulatory cell signaling pathways of mitosis can similarly turn normal cells into cancerous cells. The Gutkind Lab at UC San Diego’s Moores Cancer Center studies G-protein coupled receptors (GPCRs), which are a varied family of proteins at the center of signal transduction pathways, linking a multitude of external stimuli to corresponding cellular activity. The GPCR can receive external chemical signals at its complementary binding site, like a key in a lock. Once a chemical signal binds at the binding site, the GPCR interacts with a G-protein (G(q)) to initiate a phosphorylation cascade inside the cell, like the clicking gears in an opening lock, activating proteins called activator kinases that lead to mitosis. Curiously, research shows a high occurrence of oncogenic mutations in GPCR and G-protein associated genes in most tumor types (O’Hayre). Because the GPCR signaling pathway is essential for normal mitosis, genetic mutations producing dysfunctional proteins in
the pathway can lead to abnormal cell growth, resulting in cancer.
At the Gutkind Lab, researchers focus on mutations in G(q) and its role in the progression of uveal melanoma, a type of cancer in the eye. The lab previously concluded that gain-of-function mutations in the GNAQ, the gene coding for a subunit in G(q), lead to excessive cell proliferation (Gutkind). However, the question remains: which activator kinase is responsible?
The researchers aimed to determine which kinase was most essential to mitotic activity in cell lines as well as mouse models.
The Gutkind Lab first conducted a genomic screen across all kinase-coding genes in the cell using CRISPR-Cas9 technology to individually inactivate each gene to monitor the result of mitosis without its corresponding kinase. This approach can identify a synthetic lethal, where the presence of an oncogenic mutations in two genes, often a proto-oncogene and a tumor suppressor gene, can turn the cell
cancerous, but just one mutation will not. Synthetic lethality forms the basis of novel cancer therapy research, as any drug inhibiting the protein product of just one mutated gene will kill only cancerous cells and not healthy ones, and furthers research into targeting specific oncogenic mutations. The Gutkind Lab discovered that when a gene coding for focal adhesion kinase (FAK) was knocked out and the FAK protein was absent in the GNAQmutated pathway, cell proliferation halted despite the oncogenic mutation. FAK is a key player in regulating cell proliferation and migration or movement activity. The downstream effect of FAK showed its role in activating an oncogenic driver gene called YAP1 as well as inhibiting the HIPPO pathway that represses YAP1. Thus, by knocking out the FAK gene in a cell with a GNAQ mutation, the lab identified the FAK gene as a possible therapeutic target for treatment of uveal melanoma.
SUMOylation Modification
Genes involved in other regulatory processes beyond cell signaling can also contribute to oncogenesis. The Chen Lab, also located at UC San Diego’s Moores Cancer Center, studies SUMOylation, a process involving small ubiquitin-like modifier (SUMO) proteins. Ubiquitin and SUMO proteins are small proteins involved in post-translational modifications and the regulation of cell proliferation. In normal cells, SUMOylation is blocked when the cell senses something wrong with the DNA replication phase of mitosis, preventing cells from dividing and triggering cell death during anaphase. However, during oncogenic pathways, SUMO proteins contain a gain-of-function mutation and SUMOylation is overactivated. Because oncogenesis amplifies cell cycle progression, SUMOylation happens more frequently and acts as a key driver of cell division in cancer cells.
To observe SUMOylation in cancer cells, graduate student researchers in the Chen Lab use immunohistochemistry, a powerful technique that takes advantage of antibody-antigen interactions to detect specific antigens in cells and
tissues. Cancer cells of almost all cancer types, from blood cancer to solid tumors, have been studied to examine SUMOylation in oncogenic pathways and the cancer’s response to therapies. Using this technique, they look for SUMO proteins and the E1 and E2 enzymes, which are SUMO-activating enzymes found in all cells. According to Dr. Chen, E1 and E2 enzymes are “expressed at much higher levels in cancer cells than in normal cells.” In cancer patients, higher expression of these factors correlates with lower survival probability due to rapid oncogenesis driven by overactivation of SUMOylation.
Today, the Chen Lab focuses on developing inhibitors for SUMO proteins and the E1/E2 enzymes with hopes of decreasing SUMOylation in cancer cells and increasing longterm survival probability among patients. Through crystallography, the technique of determining the arrangement of atoms in a crystal structure, researchers recently determined the crystal structure of a complex between the E1 enzyme and a recently discovered inhibitor (C0H000). The SUMO E1 enzyme in its active conformation has specific
Active Conformation (Adenylation active)
Cys173 (Open)
Inactive Conformation
Cys173 (Open)
180° Rotation
Cys173 (Closed)
(Unbinded) COH000 (Binded)
In normal cases,the SUMO E1 enzyme is active and has residues for adenylation and the SCCH domain.When the inhibitor binds,the SUMO E1 is locked in its inactive conformation because the adenylation residues aredisordered and the SCCH domain undergoes a rotation.
Chromosomes condense and spindle-like structures form in prophase. In metaphase and anaphase,the spindle aligns thechromosomes and pulls them intoopposite poles,forming identical sisterchromatids.Separate nuclear envelopes reform in telophaseand the parent cell is cleaved intotwodaughtercells in cytokinesis. residues essential for adenylation, a biological process of attaching an adenosine monophosphate (AMP) to the protein’s side-chain, and a second catalytic cysteine half-domain (SCCH). In this active conformation, the E1 enzyme binds to SUMO proteins in its active site and adenylation happens properly. Upon binding, the C0H000 inhibitor initiates a cascade of structural changes, including a 180-degree rotation of the SCCH and disordering adenylation sites, that lock the enzyme in an inactive conformation. The inhibitor prevents SUMO proteins from binding to the E1 since adenylation can no longer occur. With these exciting discoveries, there remains hope for the development of more inhibitors for SUMO proteins to be incorporated into cancer therapies.
What Comes Next?
The research conducted at the Gutkind Lab and the Chen Lab explores the regulation of mitosis when oncogenesis occurs, and contributes to identifying inhibitor drugs through clinical trials. The Gutkind Lab studies synthetic lethal in-cell signaling pathways to target oncogenes with greater specificity for a personalized approach to therapeutics. Moving forward, the lab will continue contributing to clinical trials with different drug combinations targeting the synthetic
lethality of uveal melanoma, and also focus on the role of GPCRs in metastasis or cell migration. In the Chen Lab, researchers observed that with certain SUMO protein inhibitors, not only was SUMOylation blocked, but an antitumor response was also activated. The lab hopes to develop more SUMOylation inhibitor drugs and push them into clinical trials, to both prevent cancer cell proliferation and kill existing cancer cells in the body. As cancer research progressively focuses on
the regulation of mitosis, cancer treatments may become more effective and act as a step toward personalized medicine.
The Spinal Cord:
Our Biological Achilles’ Heel
Have you heard the story of Homer’s Achilles?
Once hailed as the greatest mythical warrior in all of Ancient Greece, he now serves as a cautionary tale to protect one’s vulnerabilities. Achilles’ vulnerability was his heel–the only part of his body not granted invincibility at birth. Similar to Achilles’ heel, we too are born with a part of our body so crucial to our being that it cannot be repaired nor replaced: the central nervous system (CNS).
written by LEANNE LIAW
AMANDA VALADEZ
illustrated by ZAID DIBIS
“The lower the NTD, the more limited functionality is”
Normally, individuals are born with a complete spine, but individuals with spina bifida are missing parts of the vertebral column causing the end of the spinal cord to develop outside of the body. (Image: Normal spine vs. various forms of spina bifida)
Composed of both the brain and spinal cord, the CNS synthesizes sensory information collected throughout the body by coordinating conscious and unconscious reactions with the brain. For instance, on a bright day, your brain might receive a message through the spinal cord that the sun is hurting your eyes. In response, your brain would send a signal through the spinal cord to direct your hands to shield your eyes from the sun. The CNS is a sophisticated system and is critical in processing and generating responses to external stimuli:, therefore any mutations or external damage to it could significantly alter a person’s quality of life.
Within the robust neuroscience research hub at UC San Diego, the Gleeson and Zheng Labs analyze cellular mechanisms for CNS deterioration at opposite ends of the age spectrum. Headed by Dr. Joseph Gleeson, the Gleeson Lab studies disease mechanisms impacting CNS development. This lab has begun to uncover how genetic anomalies result in neural tube defects within the fetuses of mothers who are low in folic acid. On the other hand, the Zheng Lab headed by Dr. Binhai Zheng studies the extent of the spinal cord’s regenerative abilities, specifically the repair mechanisms within CNS neurons.
“An estimated 10-20% of people unknowingly have hidden spina bifida”
Act I: Abnormalities & The “Gene”rosity of Fate
In embryonic development, the CNS begins as a sheet of cells until around week five, when it folds into a tube. From there, the caudal, or lower end of the tube, extends to form the spinal cord while on the opposite side, the cranial end, enlarges to form the brain. Developments within the embryo can make it challenging for the sheet of cells to fold properly. In some cases, the tube does not fully close by the end of week four, forcing
it to stay open throughout the remainder of development. Conditions where the spinal cord fails to close properly are known as neural tube defects (NTDs). NTDs are amongst the most common CNS structural abnormalities, currently affecting around 5% of all children globally.
Within this percentage, the Gleeson Lab is focusing their research on a specific type of NTD called spina bifida. Spina
bifida is a congenital neurological disorder in which the spinal cord does not close properly, inhibiting the formation of the backbone. In addition to leaving the spinal cord more exposed to extraneous dangers (i.e. accidents), spina bifida also limits the brain’s range of communication with the body. For instance, children with the most severe form of spina bifida, myelomeningocele, are born with a small pouch on their back containing part of the spinal cord, which usually limits walking and sensory capabilities.
On his mission to treat these afflicted children, Dr. Gleeson is partnering with the Spina Bifida Association (SBA) to explore the genetic and environmental implications of the condition. Years of research in the field of neuroscience have shown a pattern, although still unclear, of NTD inheritance and a correla -
tion between low levels of vitamin B9, or folic acid, and risk of developing a NTD. This suggests that there are multiple factors that lead to a fetus developing a NTD. Therefore, Gleeson and his team believe that the key to understanding spina bifida lies in examining not only the child, but the parents as well. Using trio exome sequencing, or the process of extracting and sequencing a child’s and parents DNA, the Gleeson Lab can compare their genes against one another and identify the specific ones responsible for causing the condition.
Ultimately Dr. Gleeson and his team aim to improve understanding of the genes responsible for spina bifida and develop treatments, particularly for patients with less developed spinal cords.
Act II: Resurrecting Dead Cells through Genetic Discovery
As cells age, their ability to repair their injuries greatly reduces. Spontaneous self-repair distinguishes the axons in the central nervous system (CNS) from the peripheral nervous system (PNS): PNS axons can readily regenerate, while CNS axons cannot. Axons, or components of nerve cells called neurons, act as a channel for electrochemical signals to relay sensory information to the brain and carry motor output to various parts of the body. As the central communicators to and from the brain, CNS axons that facilitate interpretation of stimuli from our environment are especially essential for survival. With this in mind, the Zheng Lab studies the molecular mechanisms behind axonal repair in the CNS and how its induction can treat patients with permanent motor function loss. Two of the Zheng Lab’s graduate student researchers, Camilo
Londoño and Kween Agba, explained how their lab began to explore these mechanisms by identifying genes that directly suppressed axon regeneration in the CNS.
In 2023, Dr. Hugo Kim attempted to regenerate axons within the corticospinal tract (CST) by silencing genes responsible for axon suppression within experimental mice. The CST was selected because of its integral role in providing voluntary movement; paralysis or other forms of limited motor function occur when axons in this path are damaged. Mice were injected in the middle of their spinal cord with one gene-specific retrograde viral tracer, which showed how information travelled to the brain through this pathway by glowing green under a microscope. This tracer also deleted genes in the CST believed to suppress
Retrograde viral tracers highlight neuron connections by injecting a colored tracer into the neuron’s synaptic terminals, which travels up the axon to also label the neuron’s cell body.
general axon regeneration. After four weeks, researchers inflicted damage in the same spinal cord region and a red gene-specific retrograde viral tracer was injected to follow the same CST pathway. Presence of the red and green tracers throughout the CST pathway meant that the CST neurons still allowed information to travel to the brain despite their injuries. Dr. Kim saw that while many neurons fluoresced either green or red, a sizable sample overlapped. These cells, categorized by neuron type, location, and gene expression, were input into a new cell identification program called a Regeneration Classifier.
Agba and Londoño posit that this Regeneration Classifier program will be an integral tool for understanding the extent of CNS neuron regeneration. As more information is added to the program’s database, research -
ers can use the program to create a spatial map of the CNS to indicate which neuronal cell types in regions of the CNS have higher regenerative capabilities. Researchers and medical professionals could match these regions to areas commonly associated with permanent musculoskeletal impairment. Regenerative axon populations in the brain could further be tracked by experimenting with mice at different ages. By seeing how these populations grow or shrink as one ages, the long term efficacy of genes coding for axon suppression can be discovered as well. If regenerative axon growth maps are created using the Regeneration Classifier program, researchers can pinpoint which musculoskeletal diseases react with gene therapy and when in a person’s life gene-based spine treatments work best.
Epilogue
The spinal cord is a powerful tool that can be permanently damaged if mishandled or malformed. While Achilles never recovered from the wounds to his heel, thanks to the Gleeson and Zheng labs, we can use our understanding of the mechanisms behind neural tube growth and CNS axon regeneration to discover how to overcome defects and injuries to this organ.
With discoveries of the spinal cord formation and regeneration on a molecular level, the health policy and pharmaceutical landscape can fundamentally change. Treatments for neural tube defects and spinal cord diseases can relieve patients and caretakers of long-term healthcare costs like rehabilitation and specialized care. Patients and their families will also be relieved of the psychological burden stemming from financial and treatment stress. While some aspects of healthcare like spinal-cord-specific rehabilitation services may decline in use, knowing how these defects and injuries form can advance fields in spinal cord academia, as well as pharmacology and biotechnology by creating new medication and prosthetics. Perhaps someday, spinal cord repair and defect prevention could be such a commonplace procedure that future generations see its current vulnerabilities like we see Achilles: a myth.
THE BIRDS and THE BEES
A Song and Dance of Communication Research
Communication is an incredibly important subject for biologists that study animal behavior, as it reveals key interactions between organisms and their environments. The way an animal communicates has implications in survival, mating, learning, adaptation, and evolution. Communication in its most basic form consists of a sender relaying a signal to a receiving group or individual with a goal in mind. This goal could be attracting a mate, alerting others of resources, or marking territory. The sender expects a certain outcome or response, while the receiver must process the signal and respond appropriately. This sender-receiver model system is how communication typically occurs in almost all organisms, whether through vocalizations, chemical messengers, or physical movement.
written by
YONHEE EU
RITA FISCHER
illustrated by LEO HARRIS
photographed by INAYA NICHOLLS
Communication behaviors are distinct and recognizable, making it easy to study them observationally. Therefore, a lot is known about the signals that animals produce, such as the vocalizations that songbirds send to attract mates or the honeybee waggle dance to communicate the location of resources to its colony. While it is important to study these signals, we cannot begin to understand why or how these behaviors occur unless we know what the signals mean, i.e. how they are processed and what behavioral response is elicited in the receiver. The Gentner and Nieh Labs at UC San Diego study these questions using songbirds and honeybees as models for understanding communication behaviors.
Birds, Brains, and Computers
Dr. Timothy Gentner, a neuroscience professor at UC San Diego, studies songbirds to bridge the neuroscience field’s understanding of communication behaviors with their underlying neural mechanisms. Specifically, his lab observes how songbirds learn, understand, and process auditory information as they receive it. Much like human speech, a songbird’s songs are not sequences of sonic events but syllabic patterns. Some birds, like starlings, have flexible vocal repertoires and communicate in ways similar to human language. For example, human understanding is more concerned with how words fit together and what they mean rather than focusing on individual words. Similarly, starlings have a vocabulary of certain sounds and pull from them to create meaning in their songs.
synthesis, which involves translating neural patterns into vocalizations of songbirds. This represents a step toward the development of advanced speech prosthetics.
Although vocal communication is common among animals, few learn during development and have such an advanced level of learned vocal flexibility, making songbirds an excellent model for studying human communication in a lab.
In collaboration with Dr. Vikash Gilja at UC San Diego’s Jacobs School of Engineering, Dr. Gentner’s lab is working to recreate a bird’s song from its neural activity. This is accomplished by recording neural traces from a region called HVc, which is responsible for learning and producing song, and a motor nucleus RA, which is needed for the motor output of song production. Mathematical models allow neural recordings to be mapped to changes in the vocal production patterns that correspond to certain sounds. The sounds can then be recreated based on the neural outputs observed. The next step for these labs is to produce signals in real time to create an artificial song while the bird thinks it is singing itself.
Dr. Gilja and Dr. Gentner are interested in how this idea can be applied to communication brain-computer interfaces
(BCIs) in humans, specifically for speech prosthetics in individuals that cannot communicate vocally. Currently, there is a lot of active research on motor-limb prosthetics and BCIs, while communication interfaces still have a long way to go. The current gold standard speech prostheses still generate frequent errors and do not grant these individuals the same vocal freedom and repertoire that most humans (and songbirds!) have.
Lauren Stanwicks, a Ph.D student in the Gentner Lab, researches communication BCIs and how sensory information integrates into pathways underlying communication in real time. In particular, she studies how animals adapt their communication vocalizations based on incoming sensory information as they speak. She hypothesizes that multiple underlying mechanisms are responsible for integrating external information into a motor output, like a vocal adjustment. For example, if you get interrupted by a loud noise while speaking, such as a car or airplane, you would naturally change your speech to accommodate this change. The same is true if you make an error while
“Dr. Gentner’s lab is working to recreate a bird’s song from its neural activity”
speaking and have to self-correct. Lauren either plays white noise at a starling to simulate an auditory interruption or puts the starling in a helium-oxygen tank, which alters the pitch of the starlings’ song, inducing a selfmade error. She records and compares neural signals from starlings as they sing, either with an external auditory stimulus or with direct manipulations to the birds’ vocalizations. Her research provides insight into how sensory integration pathways translate to vocal flexibility and adaptability, something that current communication BCIs lack.
Hive Harmony
The evolution of communication behaviors has led to remarkably complex signals like birdsong, which provides an advantage in sexual selection. Another consideration for biologists who study communication is how a given behavior functions within a society or group as a whole.
Dr. James Nieh at UC San Diego researches honeybees, an excellent model for this type of communication, thanks to their extremely sophisticated societies and efficient communication behaviors. They are eusocial, meaning that societies involve multiple generations living together, collective nurturing of young ones, and a structured system in which different groups have specialized roles. For bees, communication is key to allocating tasks, locating resources, and maintaining a healthy hive.
The honeybee ‘waggle dance’ serves as a remarkable tool for communication, as it facilitates transmission of vital details concerning resource location. At first glance, a honeybee shaking side to side seems like a simple behavior. However,
by changing features of their dance, they can convey crucial information about the distance, direction, and quality of various resources like flowers, new nest sites, or water. To encode this information accurately, dancing requires memory, precise movements, and real-time feedback. During the dance, the dancer rapidly moves her body in a figure-eight pattern. The angle of the waggle relative to the sun indicates the direction of the food source, the duration of the dance corresponds to the distance, and the number of repetitions of the dance relates to resource quality. The Nieh Lab discovered that when colonies are older and larger, bees tend to signal high quality food sources more prominently by increasing the number of runs per dance and performing shorter return phases between waggles. This adaptability ensures that the colony effectively distributes its foraging endeavors and maximizes its resource intake.
Ashley Kim, a Ph.D. student in the Nieh Lab, studies a different signal in bees called the shaking signal. While the waggle dance informs conspecifics about resources, the shaking signal reg -
ulates task reallocation among workers. Efficient task allocation is important for honeybees, as they live in colonies with thousands of individuals. The division of labor ensures the colony’s efficiency and survival in changing environmental conditions, making it an important area of study for populations that are declining due to environmental stressors. For example, during periods of heat stress, bees may need to switch from foraging
to cooling the hive. Kim uses 24-hour cameras to constantly monitor bee activity, as well as a robot that mimics the shaking signal to elicit natural responses in a controlled way. She then observes the behaviors that occur during and after a worker receives a shaking signal, its involvement in task reallocation can be better understood.
The Nieh Lab’s work also provides insights into broader biological and behavioral
paradigms. Species or population-level considerations, such as how hives adapt to environmental stressors, can be better understood through the lens of communication and social behaviors. Sociality within a honey bee colony is a testament to the complexity of nature’s communication systems, and the adaptability of organisms in response to dynamic environmental challenges.
The illustration depicts the honeybee’s waggle dance
“[Honeybees] can convey crucial information about the distance, direction, and quality of resources...”
Beyond Birds and Bees
Though the research from these two groups have wildly different approaches and applications, the underlying questions are the same: how and why do animals learn to communicate, what aspects of communication are important for relaying a message, and what happens when a communication signal is received and processed? These questions are universally important for understanding behavior, whether it is in bees, birds, humans, or other species. Studying how animals learn and adapt their behaviors for effective communication can uncover much about cognition and learning and memory pathways. Ecological interactions help to understand survival strategies and population dynamics. Finally, understanding communication’s underlying mechanisms can provide a better quality of life, through advancements in communication technology and understanding communication disorders. As the Gentner and Nieh Laboratories study the complexities of communication, they pave the way for a deeper understanding of this essential aspect of animal life.
This figure demonstrates that the duration of a honeybee’s dance indicates the distance to a food source, with longer dances signifying farther locations.
Rat Race to Recovery: Uncovering
the Secrets of Relapse
A2023 survey from the National Center For Drug Abuse Statistics reported almost one million deaths from substance abuse overdose since the year 2000, with opioids involved in at least 7 out of 10 overdose deaths. Additionally, more than 91% of people who abused opiates in the past had an episode of relapse, where a person resumes drug use after a period of abstinence or sobriety. Relapse is complicated, not only due to its nature, but because of the many ways it can occur. Social environments, mood states, and internal structural and functional changes in the brain can all potentially contribute to the onset of relapse. While there are a variety of programs and therapies available to help those experiencing relapse, there are no approved drugs to mitigate its onset.
Many people may associate addiction solely with the image of immediate and continuous drug use. However, a more nuanced perspective of addiction relies on characterizing it as not just a disease but as a conceptualization of the way the brain can change over time. Addiction, and subsequently relapse, develops through the creation of a long-lasting memory; they are not unique, isolated, and solitary experiences. Rather, the neuronal network transforms in inextricable and complicated ways, which scientists do not fully understand. Unearthing the secrets behind why addiction and relapse develop requires an understanding of neuroplasticity, the brain’s ability to constantly reorganize its neuronal network and activity in response to stimuli. As a result, many labs seek to understand the synaptic underpinnings of drug addiction and relapse, including the Martin-Fardon Lab.
written by KAREENA NARULA ADITYA VERMA
illustrated by LINDSEY KIM
photographed by DOMINIC TSE
Priming and Pathways: The Basics Behind Addiction Research
In drug addiction research, the addiction circuit pathway, though heavily studied, remains complicated. Like a racetrack where race cars travel in the same loop over and over until they cross the finish line, the reward circuit is where specialized neurons send their neurotransmitters to these in order, traveling from one brain region to another to reach their targets. An established addiction pathway in the brain flows from portions of the ventral tegmental area (VTA) to the nucleus accumbens (NAc), or the “pleasure center” of the brain. From here, these neurons eventually reach the prefrontal cortex and other areas, or the “finish line” for this circuit.
On the other hand, the onset of relapse has been explored in two facets: conditional and stress induction. Following the self-administration of a drug via a lever-press, rodents are then placed in an extinction phase, where they are weaned off of the
drug for a period of time until they no longer exhibit typical physiological signs of withdrawal such as teeth chattering, ptosis (drooping of eyelids), and body shaking. Then, they are placed in the reinstatement phase of drug seeking via drug priming, where rodents are reintroduced to a small dose of the drug to reactivate neural pathways. Here, behaviors associated with drug-seeking, drug cues or contexts, or certain stressors are assessed. Stress-induced reinstatement models are a popular choice due to a relatively simple protocol: rodents that have become dependent via self-administration of the drug are then put into an extinction phase, where they are weaned off of the drug. Then, the rodents are exposed to certain stressors, such as footshocks, and recurrent lever-pressing is assessed as a measure of relapse. Conditional-reinstatement models of drug addiction follow a similar methodology,
but have a few key differences: rodents self-administer in a certain context (i.e. environment) that contains certain and identifying stimuli. During extinction, the rodents are removed from this context and placed into another
context that does not contain the same identifying stimuli. When the rodents are introduced to the initial context again, recurrent lever-pressing is also assessed as a measure of relapse.
Dopamine Pathway
The “reward circuit” of the brain follows a typical pathway from the ventral tegmental area (VTA) and synapses at the (NAc) by releasing dopamine during the encoding of rewarding stimuli.
The
Frontrunners:
The Orexin System
At Scripps Research in La Jolla, CA, the Martin-Fardon Lab tackles many of the unsolved questions about relapse. Dr. Remi Martin-Fardon was originally interested in studying the effects of certain drugs, such as cocaine and PCP, on rodent behavior. Currently, the lab focuses on a fairly unknown yet important brain system that regulates sleep, feeding, arousal, stress, and other physiological functions: the orexin system. This neural network of substrates and receptors has piqued the interest of researchers for its potential role in characterizing the compulsive nature of drug-seeking behavior, particularly relapse. How does the orexin system help researchers
The phases of a traditional stress-reinstatement model. i. A rodent is put in an opioid-induced addiction paradigm for a select period of time. ii. the rodent is weaned off of the drug until withdrawal symptoms subside iii. the rodent is foot shocked to induce stress and the number of lever-pressed to re-receive the drug is assessed
better understand addiction and relapse? Orexins are neuropeptides secreted from the brain’s lateral hypothalamus neurons. In 2002, researchers at Vanderbilt School of Medicine discovered that the axonal projections of these neuronal orexins, or neuropeptides secreted from the brain’s lateral hypothalamus neurons, reach the dopamine neurons of the VTA. Furthermore, a 2006 study done by researchers UCSF demonstrated that when orexins can potentiate the VTA dopaminergic synapses by trafficking more NMDA receptors to the postsynaptic terminal,
highlighting their connection and potential role in the neuroplasticity of addiction and relapse. For fourth-year undergraduate Colin He, drug addiction research was an unsuspecting step forward. He, a pharmacological chemistry major minoring in general biology at UCSD, soon discovered that the Martin-Fardon Lab’s approach to research aligned closely with his interests in drug development and pharmacology research. Currently, He explores the pharmacological characteristics of Survarexit (SUV), an FDA-approved drug that treats insomnia. The lab
has previously shown that when administered orally, SUV reduces the onset of relapse in oxycodone and alcohol-dependent rats. Due to popular interest in the posterior paraventricular nucleus of the thalamus (pPVT), where orexin transmission modulates reward-seeking behavior, the lab postulates that intravenous SUV can function as an orexin receptor antagonist, meaning that SUV could potentially be used to prevent the onset of relapse in opioid use disorder by blocking orexin receptors. Under the guidance of Dr. Martin-Fardon, He and his colleagues
began assisting on a project working directly with rats under the influence of oxycodone, an opioid. There were two starting groups of rodents: one group given oxycodone, and the other given sweetened condensed milk (SCM) for comparison. He assisted investigators in setting up 21 sessions of oxycodone and SCM administration, where rats could press a lever to self-administer. Every week, the rats entered an extinction phase, where they were unable to administer the drug. After the 17th session of self-administration, the oxycodone group was then divided into two groups: the control group and the group to receive SUV. The researchers then surgically inserted a catheter implant into the pPVT to direct SUV doses to the pPVT area of the brain. To induce reinstatement to see if the rodents would display signs of relapse, the control and SUV groups of rodents were divided once again into two groups: the conditional-reinstatement (CIR) group and the stress induced reinstatement (SIR) group. The conditional-reinstatement group was placed into their original contexts (with stimuli present during the original self-administration),
and the researchers counted the number of times the rats pressed the lever to administer the drug. For the stress-induced reinstatement group, He helped give the rats a foot shock over a 15 minute timespan to induce a stress response. The results for the SIR group were recorded similarly to the CIR group.
The study found that rodents taking SUV were less likely to relapse when exposed to stress-stimuli than if exposed to context present-stimuli. These results suggest that the orexin signaling in the PVT plays an important role in the onset of relapse. While it is still unknown how exactly stress versus context stimuli alter neuroplasticity when the orexin system is blocked, these results shine light on the differing conditions that affect whether rodents will exhibit relapse, as it supports the notions that there is indeed pairing between specific stimuli and opioid use. Furthermore, these “addiction-extinction” models of relapse in rodents are useful for future research to better understand how a multitude of factors, such as rodent behavior, addiction, and memory, all play a role in the onset and prevention of relapse.
Continuing the Race?
Unfortunately, there are no successful and approved treatments for relapse available today. However, He, like Dr. Martin-Fardon, believes that his lab’s research is extremely valuable as it helps encourage future translational research efforts to test if certain FDA-approved drugs that are already on the market can potentially be used to treat relapse. Going forward, He hopes they can further expand on their work with stress and conditional-reinstatement rodent models in different brain areas connected to the orexin system. Their ongoing research delving further into the orexin system holds promise for advancing our understanding of relapse mechanisms, paving the way to continue the race for new relapse therapies.
2023 Biological Sciences student research showcase
Poster Winners
Undergradute Research
sharanya sriram
& dr. maike sander
Characterizing the Islet Cellular Landscape During Diet-Induced Progression Towards Type 2 Diabetes
Honors Research
Masters Research
xihan zhou
& dr. loren looger
Protein Engineering of Improved
Genetically Encoded Fluorescent Sensor for GABA
sienna lee schumaker
& dr. eric schmelz
Combined Gas Chromatography
Analyses of Polar and Non-Polar Metabolites From Plant Tissues
erica sarah xiong
& dr. jens lykke-andersen
The Role of the Sm Complex in TOE1
Recognition of U1 snRNAs
lili nicole follett
dr. andrew muroyama
Dissecting The Mechanistic Basis of Nuclear Migration During Stomatal Formation in Arabidopsis Thaliana
martha lok ue chow
& dr. omar s. akbari
Adapting the Population Suppression System pgSIT to the Predominant Malaria Vector, Anopheles gambiae
joseph junhyuk oh
& dr. david t. pride
Testing Antibiotic - Bacteriophage
Cooperativity in Antibiotic-Resistant Pathogens using Solid Media “Tripitaka Koreana” Stamping Method
yi chia liu
& dr. john chang
Role of Id3 On Putative Tissue
Resident Memory Precursor and Circulating Memory Precursor Cd8+
T Cell Populations
nhan albert martin dang vu
& dr. jose pruneda paz
Role of the Evening Element in the TOC1 Promoter of Arabidopsis
Undergradute Research
julian bahramipour
& dr. derek welsbie
Optimization of In Vitro Screen for Dominant Negatives of Apoptotic Dual Leucine Zipper Kinase (DLK)
akshay sridhar bharadwaj
& dr. stanley lo
Evaluating if Simple Seating Intervention
Can Foster Community Within Large Undergraduate Biology Courses
hei yu annika so & dr. alexis komor
Elucidating the Mechanisms Behind Base Editing Outcomes through Crispri Screens
adam shi
& dr. marsida kalupi
Neurobehavioral Effects of Deep Brain
Stimulation of the Nucleus Accumbens
Shell on Nicotine-Vapor Dependent Rats
gail angelica funk
& dr. christina sigurdson
Depletion of Microglial Rab7 Prolongs
Survival in Prion-Infected Mice
letian wang
& dr. yun sok lee
How Exosomes Form BMDMs
megan tiansheen hackbarth
& dr. omae mesarwi
Effect of Obesity in Metabolic and Cardiovascular Outcomes in Overlap Hypoxia
samvel sarkis gaboyan
& dr. laura crotty alexander
Fourth Generation E-Cigarettes Present Immunosuppressive Properties in Mouse Models of Allergic Asthma
ashley gabriela olvera
& dr. jerel fields
Inflammation and Effects of Cannabis
Use on HIV-related, Neurocognitive and Neurobehavioral Outcomes in PWH
katelyn elizabeth raney
& dr. suresh subramani
Investigating Novel Players that Impact Cellular Peroxisome Homeostasis
ramina mortazavi
& dr. shelley halpain
Characterization of Er F-Actin in the Somatodendritic Compartment of Hippocampal Neurons and its Role in Ischemic Stress
karthik guruvayurappan
& dr. graham mcvicker
Genome-Wide Analysis of CRISPR
Perturbations Indicates that Enhancers
Act Multiplicatively and Without Epistatic-Like Interactions
claire elise williams
& dr. sam pfaff
Moving Towards a Gene Therapy for Duchenne Muscular Dystrophy
Through RNA End Joining
lina vince lew
& dr. amy kiger
To Fly or Not to Fly: Indirect Flight
Muscle Function and T-Tubule Organization Mediated By Pi3kc2-Dynamin
Membrane Remodeling Pathway
garrett anthony ong velos danque
& dr. christina sigurdson
Role of the Evening Element in the TOC1
Promoter of Arabidopsis
shang gao
& dr. rommie amaro
Understanding Markovian Milestoning with Voronoi Tessellations (MMVT) in Simulation Enabled Estimation of Kinetic Rates (SEEKR)
jaden zhisen wang
& dr. randy hamptom
Discovering the Structural Features of Hmg2 Mallostery
Masters Research
keeley anne lanigan
& dr. carolyn kurle
Stable Isotope Analysis Suggests Two
Species Previously Believed to be Dietary Specialists are Generalists
zichen jiang
& dr. ludmil b. alexandrov
Enrichment of Pold1 Mutations in Microsatellite Unstable Colorectal Cancers
anne marie berry
& dr. radha ayyagari
Single-Nucleus Analysis of the Aging
Mouse Retina Reveals Transcriptional and Regulatory Differences In Rod and Cone Response to Aging
krista renae gerbino
& dr. justin meyer
Receptor-Binding Tropism Expansion Through the Evolution of Destabilized Intermediates In Bacteriophage 21
brandon te-hao tsai
& dr. diana rennison
Testing Assumptions in Threespine
Stickleback: Geographic and Ecological
Predictors of Phenotypic Divergence
winnie hui gong
& dr. maike sander
Establishing a Disease Model for Mody1 Using Stem Cell-Derived Pancreatic Beta Cells
taian chen
& dr. jack bui
Hydrocortisone and PMA Induce IL17D in Melanoma and Adult Primary Ear
Fibroblasts
Honors Research
chihin feng
& dr. yishi jin
Microtubule Defects Alter Neuronal Morphology and Functions in C. Elegans
zoe rebecca ford adelsheim
& dr. michael mccarthy
Role of Specific Bipolar Disorder-Associated Risk Genes in Rhythmic Gene Expression
maxwell albert gruber
& dr. christina sigurdson
Prion Protein-induced Neurodegeneration in the Central Nervous System of Drosophila Melanogaster: Building a Model
deevya shalini raman
& dr. emily troemel
Investigating C. Elegans Intracellular Pathogen Response Genes for Roles in Resistance Against Infection
gulshanbir kaur baidwan
& dr. tariq rana
Azidothymidine-induced Neurotoxicity in HIV-Associated Neurocognitive Disorders
leyi huang
& dr. jin zhang
New Fluorescent Biosensors of Protein Kinase A Activity
william drew hulsy
& dr. chi-hua chen
Analyzing and Identifying Genes that Correlate with Developmental Patterns in the Brain
allison mei christian
& dr. derek welsbie
Cloning and Purification of the S. Marcescens Endonuclease
yufei deng
& dr. tariq rana
Differential miRNAs Expressions in Anti-PD1 and Anti-CTLA4 Immunotherapy
siddharth nayan gaywala
& dr. richard daneman
The Elovl7 Gene in Brain Endothelial Cells: A Potential Modulator of Neuroinflammation
archishma srisaija kavalipati
& dr. gene yeo
Understanding Regulators and Targets of Small Nucleolar Rnas Using Enhanced Clip Data
joseph h. kennedy
& dr. terry l. jernigan
Vertex-Wise Associations with Cortical Morphology in Two Different Measures of Attention
abby chelsea lee
& dr. deborah yelon
Twist1 Genes Play Overlapping Roles in Promoting Forelimb Formation in Zebrafish
farah humam farouq
& dr. stephen leutgeb
Assessing a Potential Role of Sequential Coding for Working Memory
elise k. kim
& dr. robert rissman
Vertex-Wise Associations with Cortical Morphology in Two Different Measures of Attention
marcus kai sawamura
& dr. derek welsbie
Optimization of Recombinant AdenoAssociated Virus Production for Gene Therapy
samantha wing-kay yip
& dr. nicola allen
Delivering Astrocyte Secreted
Chordin-like 1 to Rescue Synapse Loss in Alzheimer’s Disease
anna elizabeth wilke
& dr. cory root
Intercalated Cells of the Amygdala: Connectivity and Behavioral Implications
justin wayne lam
& dr. david cheresh
Investigating Cellular Stress Responses
Mediated By Stat3 in Pancreatic Cancer
yanlin liu
& dr. yimin zou
Distribution Of Prickle Proteins In The Hippocampus Of Prickle Mutation Mice Across Developmental Stages
haoran zhang
& dr. qingfei jiang
Profiling and Interrupting the Aberrant
Rna Editing Activity In T-Cell Acute Lymphoblastic Leukemia
ashna jeetendra nisal
& dr. joseph gleeson
Role Of Folic Acid In Modulating Risk of Neural Tube Defects
shuting meng
& dr. john ravits
Investigating Sigma-1 Receptor Abnormalities in an ALS-related TDP-43 Proteinopathy Cellular Model
anita t. nguyen
& dr. varykina thackray
Investigating Effects of Antibiotic Treatment During Puberty on Anxiety and Metabolism in Adult Male Mice
celina shen
& dr. christina towers
Mitochondrial-Derived Vesicles in Cancer Cells
anqi wang
& dr. joseph gleeson
Inherited Mutation Burden Analysis for Neural Tube Defects with Wholeexome Sequencing Data
ruben benny ybarra
& dr. jody corey-bloom
Investigating Plasma Levels of Astrocyte-Associated Markers, Glial Fibrillary Acidic Protein (GFAP) and Chitinase 3-like 1 (YKL-40), as Potential Biomarkers for Huntington’s Disease
caitlyn truong
& dr. laura crotty alexander
Elevated Levels of Inflammatory Cells in Sputum and Nasal Cytology of Nicotine and Tetrahydrocannabinol (THC) E-cigarette Vapers
