Postdoctoral positions are available immediately for highly motivated individuals with an interest in molecular mechanisms underlying synaptic transmission in the lab of Dr. Jeremy Dittman at Weill Cornell Medical College in New York City (Department of Biochemistry & Biophysics). We use cutting-edge molecular and genetic techniques together with quantitative imaging, biochemical and electrophysiological approaches to probe the molecular machinery controlling fusion.
Projects focus on several critical presynaptic molecules such as complexin, Munc13, and Munc18, as well as GPCR signaling at the synapse using C. elegans as a model in vivo system together with in vitro biochemical and computational approaches. We also benefit from a highly collaborative local environment with excellent labs in our department and in the molecular biophysics program including expertise in synaptic and single-molecule imaging in cell culture, NMR spectroscopy, AFM, and lipid biochemistry. Weill Cornell is part of a vibrant tri-institutional research community including Rockefeller University and Memorial Sloan Kettering Cancer Center in the heart of New York City. Current projects focus on mechanisms by which Munc13 and Munc18 control synaptic vesicle fusion.
Some relevant past work from our goup:
Wragg, RT, Snead D, Dong Y, Ramlall TF, Menon I, Bai J, Eliezer D, Dittman JS. Synaptic vesicles position complexin to block spontaneous fusion. Neuron 2013 77(2):323-334.
Michelassi, FE, Liu H, Hu Z, Dittman JS. A C1-C2 module in Munc13 inhibits calcium-dependent neurotransmitter release. Neuron 2017 95(3):577-590.
Padmanarayana M, Liu H, Michelassi FE, Li L, Betensky D, Dominguez MJ, Sutton RB, Hu Z, JS Dittman. A unique C2 domain at the C terminus of Munc13 promotes synaptic vesicle priming. PNAS 2021 118(11).
More information is available at the lab website: sites.google.com/site/dittmanlabhomepage/
Candidates should have a PhD and ideally have experience in either biochemistry, electrophysiology, or genetics.