Michael Lin

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Michael Lin received a bachelor’s degree in biochemistry from Harvard University and a Ph.D. in neuroscience from Harvard Medical School, where he worked with Michael Greenberg. He completed his medical training at the University of California, Los Angeles, and conducted postdoctoral research in Roger Tsien’s laboratory at the University of California, San Diego. In 2009 Lin joined the faculty of the Stanford University School of Medicine. In addition to a Rita Allen Foundation award, he has received a Pioneer Award from the National Institutes of Health, a Burroughs Wellcome Fund Career Award for Medical Scientists, and a Jane Coffin Childs Memorial Fund for Medical Research Fellowship.

Lin’s research group specializes in applying structure-based protein engineering to invent new molecular tools for optical reporting and optical control of neuronal and synaptic functions. The tools they develop respond over various timescales, spanning from milliseconds to days. Tools they have invented by modifying and combining protein domains in novel ways include: (1) optical voltage indicators that are uniquely fast, responsive and two-photon-compatible; (2) optical reporters that enhance deep-tissue imaging; (3) the only completely genetically encoded method for optical control of protein interactions; (4) a general architecture for single-chain optically controllable proteins; (5) optical reporters of newly synthesized proteins; and (6) chemical controllers of new protein synthesis.

In addition to inventing molecular tools, Lin’s team has been applying these tools to previously intractable neurobiological problems. Using optical reporters of protein synthesis, they have found that the synaptic structural protein PSD95 is newly synthesized and expressed at activated synapses, and that this effect is abolished in a mouse model of Fragile X mental retardation. Interestingly, the loss of new PSD95 in the Fragile X model can be rescued by partial inhibition of the TOR pathway, implying that TOR pathway regulation may be one therapeutic approach to Fragile X syndrome.