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Sonic hedgehog (Shh) has been thought to act as a morphogen to specify different digit progenitors in the early limb bud by modulating the processing of Gli3, the major Shh signal transducer in the limb, but the immediate downstream target network critical for this is poorly understood. We are using single cell transcriptome profiling in early wild-type and mutant limb buds to characterize the initiation of different spatial zones responsive to early Shh signals. Graded Gli3 repressor function plays a major role in this early patterning, but we have found that Shh signaling is limited to a very short-range autocrine response. A position is open to investigate the molecular basis for early “digit patterning” by Gli3 modulation using a combination of genomic and proteomic approaches, including identification of Gli3-interaction partners.
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