Yimei Cai is a third-year Ph.D. student in the Department of Pharmacology and Physiology at Georgetown University. Unlike many other researchers in the field, Cai’s journey started with a teaching career. With a master’s degree in education, she taught biology for two years in local public high schools, focusing on special education. While teaching, Cai developed interests in neurodevelopmental disorders during her interactions with special needs students. After receiving her master’s degree in pharmacology, she was accepted into the Ph.D. program in pharmacology and physiology at Georgetown University.
At Georgetown, Tingting Wang’s lab uses Drosophila and mammalian models to investigate the molecular and cellular basis of homeostatic signaling in health and disease. The lab has identified several genes that are essential for glial-neuron communications in homeostatic synaptic plasticity. One of the genes identified is chromodomain helicase DNA-binding protein 2 (CHD2), which is linked to the risk of epilepsy, intellectual disability and autism. In the Wang Lab, Cai is particularly interested in the mechanisms that underlie the behavioral deficits in CHD2 mutants. She is investigating the function of Drosophila homologue of CHD2 in synapse development, synaptic plasticity, seizure behavior and sleep. Recently, Cai was selected for the prestigious Cosmos Scholars Grant program.
Principal Investigator: Tingting Wang
Fellow: Ruoxian (Susan) Huang
Undergraduate Fellow Project:
A large number of autism risk genes encode chromatin remodeling proteins, including chromodomain helicase DNA-binding protein (CHD) family genes CHD2 and CHD8. Although epigenetic mechanisms are critical for neural differentiation and learning/memory, little is known about how chromatin remodeling proteins affect brain function in a cell type-specific manner. We recently discovered that neuronal and non-neuronal CHD1, the Drosophila homologue of mammalian CHD2, plays distinct roles in regulating synaptic physiology during the induction and maintenance phase of homeostatic plasticity. However, how CHD1 expressed in different cell types contributes to the behavioral deficits in autism at the synaptic and circuit levels remains to be elucidated.
In this project, we propose to investigate the cell type-specific roles of CHD1 in regulating seizure behavior, circadian rhythm and sleep in Drosophila models. First, we will study seizure behavior, circadian rhythm and sleep in a Drosophila CHD1 genetic loss-of-function mutant. Nextwe will investigate the cell type-specific function (neuron, muscles and glia) of CHD1 in regulating different behaviors, using RNAi and tissue-specific rescue strategies. Finally, we will assess neuronal and glial calcium signals in the CHD1 mutant using genetically encoded calcium sensors and confocal calcium imaging method.