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Jeremy Kay

Assistant Professor
(919) 613-4769
Research Interest: 
Developmental biology
Research Summary: 
Molecular mechanisms of neural circuit wiring in developing retina.
Research Description: 

My lab is interested in how the events of early development influence the function of neural circuits. To address this problem we study a relatively simple circuit as a model -- the mouse retina. We are investigating how circuits devoted to specific visual processing tasks arise during retinal development, and the consequences for visual function when development goes wrong.

We seek to identify cellular and molecular mechanisms that generate different types of neurons, that endow them with specific identities, and that wire them together into circuits with a coherent function. The tools of mouse genetics are central to our approach, but we draw on a wide range of molecular, genetic, and imaging methods to tackle these questions.

MEGF10 and MEGF11 mediate homotypic interactions required for mosaic spacing of retinal neurons.
Kay JN, Chu MW, Sanes JR.
Nature. 2012. 483:465-9.

Neurod6 expression defines new retinal amacrine cell subtypes and regulates their fate.
Kay JN, Voinescu PE, Chu MW, Sanes JR.
Nat Neurosci. 2011. 14:965-72.

Retinal ganglion cells with distinct directional preferences differ in molecular identity, structure, and central projections.
Kay JN, De la Huerta I, Kim IJ, Zhang Y, Yamagata M, Chu MW, Meister M, Sanes JR.
J Neurosci. 2011. 31:7753-62.

A role for TREK1 in generating the slow afterhyperpolarization in developing starburst amacrine cells.
Ford KJ, Arroyo D, Kay J, Lloyd EE, Bryan RM, Sanes J, Feller MB.
J Neurophysiol. 2013. 31: .

Birthdays of retinal amacrine cell subtypes are systematically related to their molecular identity and soma position.
Voinescu PE, Emanuela P, Kay JN, Sanes JR.
J Comp Neurol. 2009. 517:737-50.