Labs interested in BS/MS students

With BISP 199 availabilities

Primary Investigator Contact & Info

Projects Available Desired Qualifications

Scott Rifkin

Ecology, Behavior, and Evolution


General theme

The projects in the Rifkin lab generally focus on why individuals vary in some ways but not others. For example, if you look around you'll see tons of variation between different people, but very few people have third arms growing out of their chests. Some kinds of variation are allowed by how an organism develops while other kinds are excluded. We use techniques from developmental, evolutionary, and systems biology to study the processes that generate variation and their evolutionary consequences.

Project 1

Organisms respond to environmental conditions using sets of signaling pathways where receptors sense the environment and transmit this signal through a series of protein intermediates to the nucleus of a cell where new proteins are made. There can be variation between individuals at any step in this process from how they actually sense the environment to the fidelity with which they transmit the signal to how they interpret it to how they act on that interpretation. We are using nematode worms as a model system to dissect variation in how organisms make consequential decisions about their environments. During larval life, worms decide whether the conditions are good enough to continue to reproductive development or to put their development on pause and proceed to a spore-like state called dauer until things get better. This decision is influenced by the environment (obviously) but also by genetics and randomness. The project would involve setting up and using a microfluidic and microscopy system to manipulate this decision and monitor the developmental processes that underlie it at both the organismal and molecular levels. An ideal student for this project would be someone who is interested in evolutionary or developmental biology, who likes to tinker and get devices to work, and is excited about quantitative approaches to analyzing biology.

Project 2

When two species breed, their progeny often die before completing development. However, speciation is an ongoing process and so there are cases where two species haven't completely separated and so their offspring sometimes survive. We are studying the developmental biology of species incompatibility using the nematode genus Caenorhabditis as a model system. Hybrids between different species of worms often die during embryogenesis, but some species pairs can breed and produce viable and even fertile offspring. We are tagging histones with a fluorescent protein and then using confocal microscopy to visualize the development of these worms from very early in their life and measuring where things go wrong in inviable hybrids and how their development differs from hybrids that are successful. This project involves developmental biology, evolutionary biology, microscopy, and image analysis. This project requires a student who wants to learn how to work with worms and microscopy and who is excited about learning to analyze image data.

Project 3

Developmental processes are controlled by networks of interacting genes. Often these genes are transcription factors that regulate the activity of other genes. In Caenorhabditis elegans (the model roundworm), a cell becomes a gut cell if a short network of genes culminates in the expression of a particular transcription factor that then regulates hundreds of other genes to build the gut. Despite the fact that building a gut is important if an animal is to survive, this network originated within the evolutionary history of this genus. In other words, some species that are relatively closely related to C. elegans don't build their guts in this way. We are using this set of genes as a model system to study how a new developmental network can arise and evolve. This project would involve working and measuring proteins and also measuring gene expression at single molecule resolution in some non-model organisms. This project requires a student who has experience in wet lab molecular genetics and who wants to learn image analysis. Familiarity with evolutionary biology or developmental biology would also be useful. There will also be the opportunity to learn some techniques for measuring properties of protein-DNA interactions.

Project 4

Genes interact in complex networks. Various researchers have developed simplified, computational models of gene networks they can use for in silico (in the computer) experiments. We are using one such model to study the role of gene duplication in evolution of different cell types. A student who works on this project should already have programming experience (ideally in R, Matlab, or Python) and be interested in computational and evolutionary biology.

Project 5

Water bears (a.k.a. tardigrades) are an incredible group of organisms found all over the world (look them up online!) They are around 1/2 millimeter long, can weather extreme conditions, have survived trips to outer space, and can be revived after being frozen for 30 years! Very little is known about their developmental biology. This project would involve setting up a colony of water bears in the lab and starting to look at some basic developmental biology using microscopy. This project would require someone who is intrepid and independent, who is creative in troubleshooting and tinkering with conditions and protocols and who wants to explore a relatively understudied area of biology.

Jack Bui

Medical Center Cancer Center


  1. role of IFN in promoting cancer stem cells
  2. role of the cancercell in producing cytokines and initiating immune responses
  3. role of cell-cell fusion in cancer progression
  4. role of the cytokine IL-17D in antitumor and antiviral immunity
1. need to have cell culture experience

Stephen A. Spector

Division of Infectious Disease


The Dr. Stephen Spector laboratory has used molecular and Immunologic approaches to study host-virus interactions of human cytomegalovirus (CMV) and human immunodeficiency virus type-1 (HIV-1) with a particular emphasis developing novel approaches for the detection, treatment and eradication of persistent viruses. Current CMV related research is examining the role of CMV in endothelial cell inflammation and the development of cardiovascular diseases. The laboratory has been involved with HIV/AIDS research since the beginning of the epidemic. Current research examines HIV pathogenesis with a particular emphasis on host-virus interactions, and the associations of host genetic variants on HIV diseases progression and HIV-related diseases including CNS impairment in children and adults. The laboratory has also identified specific host genetic variants that are associated with mother-to-child transmission, HIV disease progression, and antiretroviral pharmacokinetics and adverse effects. The laboratory’s interest in the identification of host factors that affect HIV pathogenesis and neurocognitive impairment led to the novel finding that during permissive infection, HIV down-regulates autophagy to promote its own replication, and the induction of autophagy (using mTOR inhibitors as well as vitamin D3) inhibits HIV replication. Most recently, Dr. Spector’s laboratory has discovered that a Na+/K+-ATPase dependent mechanism of autophagy, termed autosis, has the potential to preferentially kill HIV persistently infected cells. This research has led to him to examine the association of host factors that control HIV replication with the goal of identifying novel strategies to eradicate HIV in order to cure persons infected with HIV.

GPA- 3.5 or higher

Prashant Mali



We have several projects in the area of CRISPR-Cas based genome engineering that we are actively seeking motivated researchers for. Also here is the lab website for the students to further explore:

Frank L. Powell

Division of Physioolgy

Projects Available

Our laboratory focuses on determining the genetic and molecular signals for physiological mechanism of neural plasticity and ventilatory acclimatization to chronic hypoxia. We study healthy people from sea level and adapted to high altitude in the Andes and Tibet, as well as patients with chronic lung disease and animal models, including transgenic mice. These studies are relevant to lung disease causing chronic sustained hypoxia and chronic mountain sickness, and sleep apnea that causes intermittent hypoxia. We are especially interested in mechanisms of susceptibility and tolerance to chronic hypoxia in microcircuits that control breathing in the central nervous system.

Our recent experiments study:

  • The effects of HIF-1α versus HIF-2α in neurons versus glia for plasticity in the CNS with chronic hypoxia.
  • The role of glia and inflammatory signals in acclimatization to chronic hypoxia.
  • Identifying therapeutic targets for manipulating neural plasticity in respiratory centers arising from chronic sustained versus intermittent hypoxia.
  • Genetic determinants of individual variation in the hypoxic ventilatory response, including adaptions in human populations native to high altitude.
  • Plasticity in the control of breathing in patients with chronic hypoxemia from lung disease.

We study the problem at multiple levels, translating from genetic and molecular mechanisms to the whole animal physiology. Experimental approaches include:

  • ventilatory responses, respiratory gas exchange and functional MRI in healthy humans during acclimatization to hypoxia at high altitude, and in patients with sleep apnea receiving various treatments,

  • measuring ventilatory responses, metabolism and respiratory muscle activity in conscious, freely moving, instrumented rats and transgenic mice,

  • temporally and spatially specific conditional gene deletion using loxP-Cre strategies in transgenic mice,

  • neurophysiological studies of chemoreceptor reflexes in anesthetized rats and mice

  • in vivo and confocal fluorescent imaging, immunohistochemistry and molecular biological measures of signals for neural plasticity.

For more information please see Frank Powell's UCSD Profiles page or the Division of Physiology website

Yury Miller

Department of Medicine

The project will involve the structure-function characterization of the interaction between apoA-I binding protein (AIBP) and toll-like receptor-4 (TLR4). We have shown that AIBP regulates cholesterol trafficking in the plasma membrane and the integrity of lipid rafts, membrane microdomains that harbor activated TLR4. Cellular events following AIBP binding to TLR4 result in restraining TLR4-mediated inflammation. This mechanism is relevant to the pathogenesis of many chronic inflammatory processes, including atherosclerosis and neurodegeneration.

The student should have a strong background in biochemistry and molecular biology. S/he will learn and apply hands-on skills of molecular cloning, mutagenesis and protein-protein interactions.

Karl Willert

Cellular Molecular Medicine


Blood cancers such as leukemia and lymphoma are currently treated by replacing a patient’s supply of blood stem cells through bone marrow transplant. If we could determine how to make blood stem cells in a dish instead, we would be able to circumvent the need for bone marrow donations, which are painful and difficult to come by. The Wnt signaling pathway is known to be important for maintenance of a lot of stem cell pools, including blood stem cells. We have identified that one Wnt in particular, Wnt9a, is important for making blood stem cells. Next, we are trying to determine which other molecules in the Wnt signaling cascade modulate this effect on blood stem cells. To do so, we use a combination of in vivo biology in zebrafish, and cell biology studies in mammalian cell lines.

Jim Golden

Molecular Biology


Genetic engineering of cyanobacterial natural product biosynthetic gene clusters to understand the biosynthetic pathways and to identify the specific compounds. We also have goals of expression of the natural products in heterologous cyanobacterial strains to obtain enough of the compounds for testing pharmacological activities.

Allen F. Ryan

Departments of Surgery/Otolaryngology and Neurosciences


My laboratory performs research in the field of otology, specializing in the characterization, treatment and prevention of hearing loss.  This includes studies on the molecular mechanisms of damage to sensory cells and neurons in the inner ear, with the aim of identify potential therapies.  We also use screen compound libraries using cochlear tissue from transgenic mice in which the inner ear sensory cells selectively express GFP.  We are performing a human genome-wide association study to identify genes associated with tinnitus and hearing loss.   In addition to our neuroscience research, we study the molecular substrates of pathogenesis and recovery in otitis media (ear infections), using gene knockout models and single-cell transcriptomics to identify inflammatory and innate immune defense genes that are active in this disorder.  Finally, we investigate novel methods for drug delivery to the middle and inner ears, including a newly discovered mechanism that actively transports particles across the intact tympanic membrane.

Alessandra Franco



Human Immunology laboratory with emphasis in T cell recognition and immunotherapy design. Current focus is the role of natural regulatory T cells that recognize the heavy constant region of immunoglobulins in down-regulating inflammation.


Techniques involved: flow cytometry, culture of primary cells, ELISA.

 Maike Sander

Sanford Consortium for Regenerative Medicine


Diabetes is a complex disease characterized by the inability to control blood glucose levels. The hormone insulin is essential for blood glucose regulation, and insufficient insulin production underlies both type 1 and type 2 diabetes. Insulin is secreted into the bloodstream by pancreatic beta cells. In diabetes, beta cells fail to produce sufficient insulin due to either their destruction by the immune system (in type 1 diabetes) or an excessive demand for insulin exceeding beta cell functional capacity (in type 2 diabetes). Therefore, strategies to augment insulin production by improving beta cell function or increasing beta cell numbers have potential to restore blood glucose control in either type of diabetes.

To identify novel strategies for enhancing beta cell mass and function, we have sought to better understand how these processes normally occur during adaptation of beta cells to metabolic challenges. Prolonged changes in energy balance alter insulin demand and evoke coordinated adjustments to the number and function of beta cells. Thus, our studies have converged upon the roles of metabolic signaling in the adaptive processes of (1) beta cell proliferation and (2) enhancement of the insulin secretory response. Thus far, we have uncovered novel regulators of both beta cell replication as well as insulin secretion.

The Sander laboratory studies beta cell biology by employing genetic mouse models, animal physiology, genomics, and metabolomics. We have interrogated the roles of pathways of interest in beta cell adaptation to metabolic challenges using mouse models whose beta cells have been challenged through dietary, genetic, or pharmacological interventions. Future studies will assess the potential therapeutic value of modulating pathways of interest by investigating the effects in mouse models of diabetes. Furthermore, we will utilize genomic studies to determine the molecular mechanisms linking gene regulation to beta cell phenotypes (e.g. proliferation and insulin secretion). Through integration of our lab’s expertise in beta cell biology and genomics, we take a systems level approach to investigate the effect of gene perturbations on beta cell function.

Students will have the opportunity to play an important role in this exciting project. The student will work closely with scientists in the lab to generate mouse models of diabetes and monitor disease progression. Students will characterize various aspects of beta cell biology in these models, including determination of insulin secretion, monitoring beta cell proliferation, performing genomic studies, and assessing responsiveness to nutritional or signal transduction pathways. In parallel with mouse studies, culture models that mimic the diabetic environment will be utilized, enabling the application of cell culture tools such as CRISPR-Cas9 as well as validation in human beta cells. Through this experience, the student will learn techniques in animal physiology, endocrinology, molecular biology, and next generation sequencing. If interested, students will have the opportunity to interact with bioinformaticians to interrogate next generation sequencing data.

Previous laboratory and rodent handling experience is highly advantageous.

Nunzio Bottini


Stephanie Stanford


Clinical and Translational Research Institute

We study protein tyrosine phosphatases, enzymes that play an important role in signal transduction and are critical for numerous cellular processes in health and disease. We have projects available to study how dysregulation of protein tyrosine phosphatases contributes to autoimmunity, metabolic disorders, and cancer by causing anomalous signal transduction. The student will have the opportunity to gain exposure to cell biology, signal transduction, mouse models of disease, and the basic biochemistry of protein tyrosine phosphatases.

Jianhua Shao


Our research focuses on adipocyte biology, obesity and gestational diabetes.

Dong Wang

Skaggs School of Pharmacy and Pharmaceutical Sciences

Potential projects are:


  1. In vitro transcription studies on synthetic DNA
  2. Structure and function studies of transcription-coupled repair
  3. Structure and function studies of chromatin remodeling

Shauna Yuan

Department of Neurosciences


Astrocytes are support cells in the brain.  Although astrocytes harbor pathological hyperphosphorylated tau and neurofibrillary tangles, hallmarks in neurodegenerative diseases, how they contribute to disease is not clear.  This project is to investigate tau phosphorylation and tau splicing in human astrocytes.  We have preliminary results, which show that tau phosphorylation and tau splicing in astrocytes are significantly different from neurons, suggesting that the mechanisms regulating tau protein modification is different in astrocytes than neurons.  These important questions will be answered by comparing human astrocytes and neurons derived from human induced pluripotent stem cells.  The student will learn to cultures human astrocytes and neurons, quantitative PCR, immunofluorescent staining, and Western blot.  

Hollis Cline

Department of Neuroscience


Our research is focused on understanding the mechanisms by which experience controls the development of the brain. The lab addresses this fundamental neuroscience question by examining the development of the visual system in Xenopus tadpoles, which is well known for its experience-dependent plasticity. Using in vivo imaging, electrophysiology, behavioral assays, and manipulation of gene expression, we have discovered that neuronal activity regulates the development of the visual system through a variety of mechanisms, including changes in neuronal structure, synaptic strength, synaptogenesis, and gene expression.

 The tadpole visual system is highly dynamic and We have shown that animals can recover visually-guided behaviors after brain injury. We are investigating the response to injury.

We have 3 types of projects. 1: students will use the tadpole system to study mechanisms controlling recovery from brain injury. Students will be exposed to methods including whole-brain electroporation, in vivo imaging, immunofluorescence, molecular biology, biochemistry, tadpole husbandry, and general lab techniques. They will learn animal behavior assays and analysis as well. 2: students will participate in a project on computational bioinformatic analysis of RNA Seq data from Xenopus brain tissue. 3: students will participate in a project investigating visual response properties using electrophysiological or imaging methods and quantitative data analysis. Students will be part of a dynamic group of scientists seeking to understand the fundamental aspects of cellular neuroscience using modern molecular techniques and state of the art technology.

Tariq Rana

Pediatrics and Genetics


Research opportunities are available in a multidisciplinary laboratory studying fundamental questions in chemical and RNA biology. Ongoing projects include: (1) Bioinformatics and systems medicine using HT genome sequencing of blood cells from cancer and AIDS patients. (2) CRISPR-Cas9 applications in genome engineering. (3) Developing new approaches for cancer immunotherapies.

 Additional Info: Under supervision of a postdoctoral fellow or a staff scientist, you will be exposed to: bioinformatics analyses of large genomics data sets, culturing and differentiation of stem cells, drug discovery, viral transduction, RNA and DNA isolation, PCR and gel electrophoresis, transfection, western blot, in vivo and in vitro cancer models, and lab maintenance.

Must have a strong desire and commitment to perform scientific research in human disease mechanisms. Must have an understanding of biochemistry, bioinformatics, chemistry, cell biology, or molecular biology. Prior lab experience is a plus.

Documents to Submit: Resume, Cover Letter, Unofficial Transcript

Huilin Zhou

Department of Cellular and Molecular Medicine

Title of the project: The SUMO pathway for genome maintenance. 


Also see for further details. 


Karl Willert

Cellular and Molecular Medicine


The Big Picture: A central question in developmental biology is how cells in an embryo become different from one another. Many years of research have shown cellular diversity arises as a consequence of cells interacting with their immediate environment and receiving instructive signals from neighboring cells and the extracellular matrix. Like the developing embryo, human pluripotent stem cells (hPSC) maintained in the laboratory communicate with one another using signaling molecules and thereby either maintain their pluripotent state or assume new properties. Recreating the cellular microenvironments and reiterating the developmental signaling events by controlling the dosage, timing, and combinations of developmental signaling molecules is of critical importance in establishing protocols for reproducible generation, expansion and lineage specific differentiation of hPSCs.

What We Study: In my laboratory we study a major class of signaling proteins encoded by the WNT gene family, which exerts potent effects on stem and progenitor cells. Despite a vast body of research on the role and mode of action of WNTs in developmental biology, how these signaling proteins control cell fate choices of hPSC is poorly understood.  A long-term goal of the lab is to develop methods and protocols to specifically manipulate stem cell fate with WNT proteins, thereby providing the means to derive and isolate mature cell populations. 

The Lab Environment: The Willert laboratory is located in the Sanford Consortium for Regenerative Medicine (SCRM), where over 25 PIs with stem cell interest have established their research programs. At present, 8 full time scientists work in the Willert lab: one post-doc, two Ph.D. students, two Masters student, and 3 lab technicians. In addition, two undergraduate students work in the lab on a part-time basis. We have weekly lab meetings at which individual lab members present their research progress and future plans. SCRM offers a highly interactive environment with several scientific seminar series.

Potential Projects:

  1. Protein engineering. WNT proteins are potent stem cell factors that, depending on cellular context, promote self-renewal or differentiation. However, WNT proteins are difficult to isolate as bioactive molecules, which has limited their usefulness in cell and tissue engineering. We have developed approaches to overcome these obstacles by engineering novel WNT-like proteins. A student working on this project will learn how to purify proteins and test activities on hPSCs.
  2. WNT signaling in blood development. Blood stem cells are widely used in the clinic to treat a variety of incurable diseases, however, supplies of patient-matched blood stem cells are limited. Developing protocols to generate blood stem cells from hPSCs would be revolutionary in regenerative medicine. Using zebrafish as a model system we found that a specific Wnt gene is required for proper blood stem cell development (Grainger et al. Cell Reports, 2016). Furthermore, we found that this WNT requirement is conserved in humans (in press). A student working on this project will have the opportunity to work with human pluripotent stem cells and differentiate them towards blood lineages.
  3. The role of FZD7-WNT signaling in stem cells and cancer. We have found that the WNT receptor FZD7 is required for maintenance of hPSCs in a pluripotent state (Fernandez et al. PNAS, 2014). In the course of these studies, we developed an antibody to FZD7, which inhibits WNT signaling through this receptor. FZD7 has also been found to have important roles in cancer, and our antibody represents a unique opportunity to block cancer growth. An intern working on this project will have the opportunity to work with human pluripotent stem cells and human cancer cells and test the hypothesis that disruption of WNT-FZD7 signaling blocks stem and cancer cell growth.

The only requirements I have is that a student can commit a minimum of 1 year (preferably longer) to my lab and that they are interested in and excited by research.

Chengbiao Wu



  1.  Mechanisms of cortical-striatal atrophy in HD


    We focus on the investigation of axonal trafficking and signaling of BDNF in mouse models of Huntington's disease (HD). Our studies have demonstrated that defective axonal transport of BDNF in cortical neurons contributes significantly to striatal atrophy in HD. More importantly, we have shown that TRiC chaperonin has a protective role against axonal toxicity induced by mutant Huntingtin. 

    2.  Axonal dysfunctions in Tauopathies.

    Tau is a microtubule associated protein (MAP). Hyper-phosphorylation or mutations in many sites on Tau are believed to contribute to its significant neurotoxicity.  Using human neurons differentiated from iPS cells derived from human Tauoapthy patients, we are interested in understanding:  1: how pathogenic Tau species affects axonal transport of neurotrophic factors such as BDNF;  and 2: if and how pathogenic Tau can spread via axons from neurons to neurons, or from glia to neurons, or vice versa

    3.  Molecular and cellular mechanisms of CMT2B peripheral sensory neuropathy

    Charcot-Marie-Tooth disease type 2B (CMT2B) is caused by autosomal dominant mis-sense mutations of the small GTPase Rab7 in people. We will investigate, both in vivo and in vitro, the hypothesis that CMT2B Rab7 mutation(s) causes hyper-activation of Rab7 and disrupts axonal trafficking and signaling of neurotrophic factors, leading to axonal degeneration of peripheral sensory neurons. The hypothesis is built on our in vitro studies published previously (Zhang et al., 2013, J Neurosci. 33:7451-62); and our strong preliminary in vivo results of the first ever mouse model of CMT2B, demonstrating sensory dysfunction in a knockin mouse model. In addition, we have obtained human CMT2B fibroblasts together with their control cells.  We plan to convert these cells into sensory neurons using the recently developed technologies by our collaborator Dr. K Baldwin at TSRI. By carefully examining the animal model, studying the cellular and molecular mechanisms in both animal neurons and human neurons, we will gain significant insights into the pathogenic mechanism(s) of CMT2B towards potential therapies for this debilitating disease.

    4.  Molecular and cellular mechanisms of HSAN V

    Hereditary Sensory and Autonomic Neuropathy V (HSAN V) is associated with a naturally occurred autosomal recessive mutation in NGF, discovered in a Swedish family whose patients suffer from selective loss of sensation to deep pain.  In this project, we will investigate and characterize the signaling mechanisms of this novel NGF mutant both in vitro and in vivo.  We will study how the mutation alters NGF’s ability to signal through TrkA and/or p75.  Our preliminary studies support the hypothesis that the mutant NGF retains its ability to signal through TrkA while no longer engaging the p75-mediated signaling pathways. We are actively exploring the potential use of this novel NGF mutant for treating peripheral sensory neuronal degeneration such as diabetic neuropathy, CHEMO- and HIV-induced neuropathy.


Stephen Spector


 The Dr. Stephen Spector laboratory has used molecular and Immunologic approaches to study host-virus interactions of human cytomegalovirus (CMV) and human immunodeficiency virus type-1 (HIV-1) with a particular emphasis developing novel approaches for the detection, treatment and eradication of persistent viruses. Current CMV related research is examining the role of CMV in endothelial cell inflammation and the development of cardiovascular diseases. The laboratory has been involved with HIV/AIDS research since the beginning of the epidemic. Current research examines HIV pathogenesis with a particular emphasis on host-virus interactions, and the associations of host genetic variants on HIV diseases progression and HIV-related diseases including CNS impairment in children and adults. The laboratory has also identified specific host genetic variants that are associated with mother-to-child transmission, HIV disease progression, and antiretroviral pharmacokinetics and adverse effects. The laboratory’s interest in the identification of host factors that affect HIV pathogenesis and neurocognitive impairment led to the novel finding that during permissive infection, HIV down-regulates autophagy to promote its own replication, and the induction of autophagy (using mTOR inhibitors as well as vitamin D3) inhibits HIV replication. Most recently, Dr. Spector’s laboratory has discovered that a Na+/K+-ATPase dependent mechanism of autophagy, termed autosis, has the potential to preferentially kill HIV persistently infected cells. This research has led to him to examine the association of host factors that control HIV replication with the goal of identifying novel strategies to eradicate HIV in order to cure persons infected with HIV.

What type of activities will you assign to your research assistant?

FMP students will work closely with a postdoctoral fellow or Research Scientist in the laboratory. Students will learn how to grow cells in culture and basic molecular biology techniques including extraction of DNA, RNA and proteins, PCR, western blots, immunostaining, etc. It is hoped that by end of the first semester students will have learned sufficient techniques to begin working on their own research project under the guidance of Dr. Spector and their direct laboratory research mentor. Many students have gone on to complete a Master’s thesis in the laboratory as part of the BS/MS program before entering medical school or pharmacy school.


Students must have a GPA of 3.5 or higher to be considered for the lab.

Asa Gustafsson

Skaggs School of Pharmacy and Pharmaceutical Sciences


Our lab is interested in understanding the signaling pathways that regulate mitochondrial function and turnover in cardiac myocytes. Defects in these pathways contribute to loss of cardiac myocytes and development of heart failure.  Cardiac myocytes are highly active cells that require large amounts of energy supplied by mitochondrial oxidative phosphorylation. Since mitochondria are critical to myocyte function, it is not surprising that there is a strong link between mitochondrial dysfunction and cardiovascular disease. Defective mitochondria can also activate of cell death pathways which can lead to loss of cardiac myocytes and reduced ability to sustain contractile function. This ultimately contributes to the development of heart failure. Therefore, the ability of the cell to overcome mitochondrial damage requires removal of the impaired mitochondria via autophagy.Autophagy is an evolutionarily conserved process involved in the degradation of long-lived proteins and organelles.

 Project #1: The E3 ubiquitin ligase Parkin plays an important role in labeling dysfunctional mitochondria for degradation in cells. Parkin is normally localized in the cytosol but rapidly translocates to damaged mitochondria to promote their degradation by ubiquitinating proteins in the outer mitochondrial membrane. The ubiquitin serves as a signal for autophagic degradation.   This project will explore  the mechanisms underlying Parkin-mediated clearance of mitochondria in cells. 

 Project #2:  MCL-1 is an anti-apoptotic Bcl-2 protein which is expressed at high levels in the heart compared to other anti-apoptotic Bcl-2 proteins. However, very little is known with respect to how MCL-1 regulates cell survival in cardiac myocytes. We have discovered that cardiac specific deletion of MCL-1 lead to  mitochondrial dysfunction and rapid development of heart failure, suggesting that MCL-1 is critical for myocyte survival.  We have found that one function of MCL-1 is to promote degradation of damaged mitochondria.  In this project, the student will investigate the molecular mechanisms by which MCL-1 regulates mitochondrial clearance in cells.


Jim Golden

Molecular Biology


Please see link for information regarding projects:


I prefer students that are not yet in their final senior year and that have taken genetics and molecular biology.

Stephanie Stanford

Clinical and Translational Research Institute


Nunzio Bottini

Clinical and Translational Research Institute


Biochemical assessment of a tyrosine phosphatase involved in immune-mediated diseases


Biochemical assessment of a tyrosine phosphatase that promotes cancer progression.


Chitra Mandyam

Department of Anesthesiology


Our research is focused on understanding the mechanisms by which addiction to illicit drugs and alcohol affect brain stem cells and their function.
Our lab addresses this emerging neuroscience question by using high profile behavior models that mimic abuse and dependence to methamphetamine and alcohol. We use operant self-administration addiction models combined with biochemistry, histology, electrophysiology and learning and memory functions to determine the role of neural stem cells and glial progenitors in the adult mammalian brain in the pathophysiology of addiction.
We have 3 types of projects: We have recently discovered that newly born neurons in the hippocampus via a process called neurogenesis during abstinence from drug contribute to or enhance propensity for relapse. We are currently doing experiments using transgenic rats and genetic approaches to determine the neural circuitry underlying this maladaptation in the hippocampus.
We have also discovered that nonneuronal cells in the prefrontal cortex play a role in disturbing neuronal plasticity and promote relapse to alcohol seeking. We are currently doing experiments using transgenic rats and pharmacological tools to determine the functional significance of oligodendroglial cells and endothelial cell adhesion molecules in the prefrontal cortex in relapse to alcohol seeking.
In collaboration with Dr. Brian Head and Dr. Hemal Patel in the department, we have recently discovered that the membrane/lipid raft protein Caveolin-1 in the dorsal striatum may play a role in reinforcing properties of the psychostimulant methamphetamine. Ongoing experiments will determine the functional significance of this protein in methamphetamine addiction and discover new avenues to treat addiction.
Students will be exposed to animal behavior, biochemical studies including Western blotting, histology including immunohistochemistry, stereology and electron microscopy and electrophysiological studies including slice physiology.

Must have a GPA of 3.5 or higher, must be motivated to do basic science research; must have an understanding of biochemistry and cell biology. Previous lab experience is not necessary but welcome.
Please Submit: Resume, Cover Letter, Unofficial Transcript

David K. Welsh


Department of Psychiatry

Project related to circadian rhythms in brain cells, and relation to depression-like behavior in mice.

Some lab experience who has taken the basic undergrad Circadian Biology course

 Joanne Chory

Plant Biology Laboratory

SALK Institute

Project 1:  Heat stress and global warming of plants

Environmental stresses such as heat and drought have adverse effects on plant growth and crop yield. Heat stress is one of the major abiotic stresses to plants and it now occurs more frequently as a consequence of global warming. This project will use genetic screening and molecular biology methods to identify genes that are involved in chloroplast signaling-controlled plant heat stress response pathways. We have already isolated some mutants resistant to heat stress and next work will be mainly focused on assaying the phenotypes of the mutants, mapping corresponding mutated genes from the mutants using high-throughput sequencing technology and validating gene functions. The major lab techniques will include: plant management, sample collection, plant crossbreeding, genotyping, seeds collection as well as molecular biology experiments like gene cloning, PCR, next-generation sequencing and data analysis. More detailed experiments will be set up based on the research progress of the project. You will work with and be supervised by a postdoc research associate in the lab.

Project 2:  Protein kinase function in plant temperature responses

This project will examine the role of an uncharacterized protein kinase in light and temperature responses in the model plant,   Arabidopsis thaliana. This kinase is related to well-characterized genes in animals. As this gene has not previously been studied in plants, the initial steps of the project will be constructing and confirming molecular and genetic tools. The student will generate transgenic plants expressing mutant versions of the kinase, with the possibility of generating novel alleles using the CRISPR-Cas9 system. These and other tools will be used to characterize physiological responses to environmental light and temperature conditions, and examine possible genetic or biochemical interactions with known pathways. This work will be performed under the mentoring of a postdoctoral fellow in the Chory laboratory.


Paula Desplats

Department of Neuroscience

1. Dynamic DNA methylation and circadian alterations in Alzheimer's disease.

Disruptions in circadian regulation are a prominent clinical feature and a major factor of hospitalization and morbidity in Alzheimer's disease (AD). We recently uncovered alterations in the expression of the circadian clock gene BMAL1 in patient-derived fibroblasts and postmortem brain samples from early and late AD cases, associated with aberrant patterns of DNA methylation ( Cronin et al 2016, Alz & Dementia). We are currently investigating the mechanisms that regulate cyclic methylation and how these become altered in AD.

Exploring the impact of circadian alterations in neuronal physiology we also identified Insulin Degrading enzyme (IDE), involved in both, insulin signalling and amyloid-b clearance, as a circadian output directly regulated by BMAL1. We are investigating IDE regulation and its role in brain insulin resistance in AD.

2. Role of DNA methylation on modulating inflammation in Alzheimer's disease.

Neuroinflammation correlates with onset of AD and cognitive decline, and it is implicated in the pathological cascade leading to amyloid plaques. The role of epigenetic mechanisms on modulating inflammation is yet poorly understood. My current research seeks to identify alterations in DNA methylation on inflammation-related genes that may contribute to AD.

We recently completed genome-wide methylation analysis on postmortem frontal-cortex samples from subjects with AD and mild cognitive impairment (MCI) and identified multiple differentially methylated genes associated with immune response and inflammation. Using human primary microglial cells as in vitro model we are currently investigating imbalances in methylation enzymes and applying CRISPR/Cas9 technology to attempt epigenetic editing of inflammatory targets.

3. Alterations in autophagy-regulating miRNAs and oligodendroglial accumulation of a-synuclein in Multiple Systems Atrophy (MSA).

After identifying miR101 as an autophagy-regulating microRNA altered in MSA brains we are now interested in understating how changes in miRNAs that regulate vesicle sorting and autophagy contribute to pathological accumulation of a-synuclein in oligodendrocytes in MSA. Pairing my expertise in proteostasis and epigenetics with Regulus Therapeutics, an industry leader in miRNA therapy, we are evaluating the potential of modulating autophagy-inhibiting miRNAs to reduce a-synuclein accumulation as a therapeutic approach for this devastating disease.

GPA 3.5 or higher

Hands-on experience (by working on previous lab) in at least one of the techniques below:

1. Cell culture

2. Western blot and protein extraction

3. RNA isolation and qPCR

4. DNA isolation / cloning / minipreps

5. Immunohistochemistry / microscopy

15 h /week minimum dedication