Postdoctoral Fellows

Y Badawi Yomna Badawi Ph.D., Postdoctoral Fellow
Mentor: Hiroshi Nishimune

Amyotrophic lateral sclerosis (ALS) patients and animal models show denervation of neuromuscular junctions (NMJs), which is a dying-back neuropathy. However, the etiology of ALS and this neuropathy is not known, and interventions are lacking. My research focuses on the evaluation of exercise and stem cells for the amelioration of NMJ denervation in ALS models.
Soumita Dutta, Ph.D., Postdoctoral Fellow
Mentor: Prachee Avasthi

Research Interest: Chlamydomonas reinhardtii has long been used as a model organism in studies of cell motility and flagellar dynamics. Understanding the mechanism involved in flagellar dynamics and investigating the biology of ciliary/flagellar proteins are critically important for identifying sources of ciliopathies including primary cilia dyskinesia, poly cystic kidney disease, polyductyly, male infertility and even cancer. New studies on Chlamydomonas indicate that actin is one of the key players in regulating the IFT machinery to control assembly/disassembly of flagella and to control flagellar length. However, the mechanisms involved are largely unknown. My research focuses on modification of actin’s dynamics with the ciliary dynamics which ultimately provides broader opportunities for understanding the basic biology of the cilia-related disorders and their therapeutic approaches.
D. Jacobs Damon Jacobs Ph.D., Postdoctoral Fellow
Mentor: Pamela Tran

Research interest: Obesity is a growing epidemic in industrialized nations of the world and is the primary cause of several life-threatening metabolic disorders, such as hypertension, liver disease, and diabetes. Primary cilia are antennae-like extensions present on most cells of the body, they contain receptors (such as Hedgehog, Wnt, PDGFa, ...etc.) that are important for communicating signals from the extracellular environment into the cell. ‘Ciliopathies' arise due to defects in proteins that localize to primary cilia and can cause developmental and postnatal defects such as polydactyly, cystic kidney disease and obesity. Thm1 is a critical ciliary protein that is important in maintaining proper cell signaling programs, and I am working with a THM1-/- mouse model to characterize the postnatal obesity phenotype and examine the physiological and neurological causes of obesity onset. We are working toward identifying potential therapeutic targets for controlling the onset of obesity.
Robert Rogers, Ph.D., Postdoctoral Fellow
Mentor: Hiroshi Nishimune

Research interest: As more individuals are living to more advanced ages, loss of muscle function and mass occurs as a result of changes in innervation of the neuromuscular junction (NMJs). The molecular mechanisms leading to the progressive loss of NMJ innervation during aging have not been well characterized. Furthermore, one of the best preventative practices to prevent the loss of muscle strength during aging is exercise. My research centers around mechanisms by which the NMJ remodels with aging resulting in a loss of innervation and how exercise prevents this loss. I also have a strong interest in metabolic diseases, such as insulin resistance and type 2 diabetes, that frequently occur concurrently during aging.

Last modified: Jun 13, 2016