Postdoctoral fellow jobs and graduate student rotation projects are available. Contact Dr. Yongchao Ma for details.
Regulation of Mitochondrial Function in Motor Neuron Degeneration
As the leading genetic cause of infant mortality, spinal muscular atrophy (SMA) affects one in every eight thousand live births. Amyotrophic lateral sclerosis (ALS) or Lou Gehrig’s disease is the most common motor neuron disease in adults. Both SMA and ALS are characterized by the selective degeneration of spinal motor neurons. Our group is interested in studying mechanism regulating motor neuron development and function, as well as why motor neurons specifically degenerate in SMA and ALS. To address these questions, we use a combination of genetic, biochemical and cell biological approaches, and utilize genetically modified mice, induced pluripotent stem (iPS) cells reprogrammed from fibroblasts, and zebrafish as model systems. We focus on the regulation of mitochondrial functions in SMA and ALS pathogenesis. Based on our findings, we hope to develop new therapeutic strategies for treating these diseases.
Regulation of Neural Stem Cell Development and Neurodegenration by RNA methylation
Biological functions are determined by protein expression, which is modulated by various post-transcriptional regulations of RNA. RNA methylation on N6-adenosine is emerging as a critical regulator of RNA functions and metabolism. We recently identified novel m6A RNA readers that interpret RNA methylation to regulate different aspects of RNA biology, including RNA localization, degradation and translation. We are exploring how RNA methylation regulates fundamental aspects of neural development and degeneration such as neurogenesis, neural stem cell differentiation, neuroinflammation, and how dysregulation of these processes contributes to the pathogenesis of autism, ALS and other neurological disorders.
Aging and Mitochondrial Oxidant Defense in Dopaminergic Neuron Degeneration of Parkinson’s Disease
Dopaminergic neurons located in the ventral midbrain control movement, emotional behavior and reward mechanisms. Dysfunction of these neurons is implicated in Parkinson’s disease (PD), drug addiction, depression and schizophrenia. Our group is interested in the genetic and epigenetic mechanisms regulating dopaminergic neuron functions in disease and aging conditions. We are particularly interested in how aging and mitochondrial oxidative stress contribute to dopaminergic neuron selective degeneration in PD through transcriptional and epigenetic regulations. We use mouse models, cultured neurons and iPS cells for these studies.