Current TL1 Trainees

George Campbell, B.S.

The microtubule-based motor proteins kinesin and dynein mediate the anterograde and retrograde active transport of cargos in axons, respectively. This transport is highly regulated and essential to axonal health and function. The importance of understanding vesicular transport mechanisms is furthermore highlighted, as there is evidence that disruptions in axonal transport could be involved in the initiation of neurodegenerative diseases such as Alzheimer’s and prion diseases.

As a TL-1 trainee, George investigates how protein aggregates induced by infectious prions inside axons may lead to axonal blockages and to impairments in synaptic vesicle transport that can lead to neuronal dysfunction. Elucidating the mechanisms of how motor proteins regulate transport and how transport is specifically impaired in prion diseases will allow the design of therapies to directly target motor protein dysregulation and thus “dissolve” traffic jams created by prion aggregates. Thus, we will use knowledge gained from motor regulation in healthy neurons to treat motor dysfunction in prion and other neurodegenerative diseases.

Prior to his graduate studies at TSRI, George was awarded a B.S degree in both Biology and Chemistry at the University of Tennessee at Chattanooga in 2011. Previous research experiences include summer research in biochemistry and an undergraduate thesis in genetics.

Nicholas Jacob, B.S.

Over the past decade, contributions of inflammation and effects of the immune response in cancer growth and metastasis have become greatly appreciated. While some immune effectors work to eliminate neoplastic growth, malignant disease evolves to circumvent these factors and even utilize them for growth and proliferation. As a TL1 trainee, Nick uses small-molecule modulators of immune functions as probes to study the tumor-immune microenvironment and break the resistance of cancer to clearance by the immune system. The hope is this work will uncover new receptors for targeted therapy and even new drugs for cancer treatment.

Nick is also involved with designing vaccine formulations for the treatment of narcotic addiction.

Prior to his graduate studies at TSRI, Nick received his B.S. in chemistry from the University of Rochester in NY. He completed his undergraduate research thesis and a NSF REU under Prof. Rudi Fasan on the design and synthesis of unnatural amino acids used in the biosynthesis of macrocyclic organo-peptide hybrids for the selective targeting of protein-protein interfaces.

Margarete Daisy Johnson, M.S.

Margarete Daisy Johnson Chronic wounds, including pressure sores and diabetic ulcers, are a common and increasing clinical problem for which improved treatment strategies are needed. γδ T cells, which are known to contribute to the wound healing response, are found in an unresponsive state in chronic wounds. Interactions between JAML (junctional adhesion molecule-like protein), a protein on the surface of γδ T cells, and the coxsackie and adenovirus receptor (CAR) on keratinocytes provide a costimulatory signal to γδ T cells functionally similar to CD28/B7 interactions in traditional αβ T cells. The CAR protein is upregulated in acute but not chronic wounds, making the JAML/CAR interaction a promising target for reactivating unresponsive γδ T cells.

As a TL-1 trainee, Daisy is investigating how the JAML/CAR interaction can be utilized to reactivate these unresponsive cells. In order to deliver the CAR molecules into wounds, the Havran lab is collaborating with the Finn lab at Georgia Tech to embed the proteins in degradable hydrogels that will allow for their finely tuned, timed release into damaged tissues.

Before coming to TSRI, Daisy received a B.S. in biology from Cornell University where she completed an honors thesis on the evolution of defensive traits in the stem succulent genus Pachypodium. She then completed an M.S. in biomedical sciences at Texas A&M University with a thesis “designing an in vitro model for equine laminitis and investigating the role of apolipoprotein A-IV in the disease.”

Alyson Smith, B.A.

Myosin-IIA is an actin-binding motor protein that is present in diverse cell types, where it is essential for cell shape, polarity, adhesion, and migration. Mutations in the myosin-IIA heavy chain (MYH9) lead to a number of rare, autosomal dominant inherited disorders known as MYH9-related diseases. The most severe and well-studied effects of these diseases occur in cells in which myosin-IIA plays a critical, non-redundant role, such as megakaryocytes, which form platelets, and the podocytes of the kidney. However, the effects of MYH9 mutations in other cell types and the mechanisms by which these mutations cause disease are not understood.

As a TL-1 trainee, Alyson investigates the function of myosin-IIA in red blood cells and the ways in which MYH9-related diseases disrupt this function. Her research aims to test whether myosin-IIA interacts with the red blood cell membrane skeleton, which is a network of short actin filaments interconnected by long spectrin strands that underlies the plasma membrane. This interaction could regulate the shape, flexibility, resilience, and membrane subdomain organization of red blood cells in the circulation. This research will increase understanding of the pathology of MYH9-related diseases and the molecular mechanisms that cause them, which can inform new therapies for these diseases and other disorders that affect the actomyosin cytoskeleton.

Prior to her graduate studies and TSRI, Alyson earned a B.A. degree in Molecular and Cell Biology with an emphasis in Genetics, Genomics, and Development at the University of California at Berkeley in 2013. Her undergraduate research focused on the genetic and developmental basis of skeletal evolution in the threespine stickleback fish.

Louis Gioia, B.A.

Kidney transplantation is the best treatment option for most patients with end-stage renal disease. As such, thousands of kidney transplants are performed each year in the United States, representing over half of all organ transplant procedures. Advancements in post-transplantation immunosuppressive therapies have greatly improved short-term transplant survival rates, but long-term organ survival is still a major issue. A better understanding of the biological processes behind long-term kidney transplant rejection will allow for better prediction and monitoring of transplant outcomes.

As a TL1 trainee, Louis uses bioinformatics approaches and next-generation sequencing to decipher the biological processes controlling long-term kidney transplant rejection, while also creating tools for the prediction and monitoring of these underlying processes. By studying the genomes of large cohorts of kidney transplant patients, Louis hopes to identify the genetic factors responsible for the rejection of transplanted kidneys. With a more detailed picture of how and why kidney transplants fail over time, physicians will be better able to maximize the utility of each transplantation procedure.

Prior to his graduate studies at TSRI, Louis received a B.A. in Biology from Washington University in St. Louis. As an undergraduate, Louis worked in the laboratory of Ursula Goodenough, PhD, investigating lipid biosynthesis in green algae for the optimization of algal biodiesel production.

Siddhartha Sharma, M.A.

Siddhartha Sharma Ulcerative colitis (UC) is the most common form of Inflammatory Bowel Disease (IBD). Though it is most prevalent in North American and European populations, it is growing worldwide. While genome wide association studies have identified a number of loci that are UC specific, genetic inheritance can only account for a portion of the increase in disease incidence. This point is best exemplified by the fact that there is only a 10-15% concordance rate of UC between monozygotic twins. Thus, it is important to consider the role of epigenetics in UC.

As a TL1 trainee, Siddhartha’s research aims to improve our understanding of the role of epigenetics in acute UC. Having a better understanding of the epigenetics and underlying molecular interactions may help improve molecular diagnostics as well as therapy management for UC and related inflammatory conditions.