Abstract
During vulval development in Caenorhabditis elegans , a signal arises from an anchor cell that activates the mitogen-activated protein kinase (MAPK) pathway to specify cell fate of three vulval precursor cells, with primary fate affected in the P6.p cell and secondary fate in the adjacent P5.p and P7.p cells. Berset et al. show that two different vulval cell fates are produced in adjacent cells through the action of two antagonistic signaling pathways. Upon activating the MAPK pathway, the primary fate of P6.p is induced. A lateral signal moves out from P6.p that increases expression of NOTCH in P5.p and P7.p. NOTCH turns on the MAPK phosphatase gene lip-1 . LIP-1, in turn, blocks MAPK activity in P5.p and P7.p and allows the secondary cell fate to develop. T. Berset, E. F. Hoier, G. Battu, S. Canevascini, A. Hajnal, Notch inhibition of RAS signaling through MAP kinase phosphatase LIP-1 during C . elegans vulval development. Science 291 , 1055-1058 (2001). [Abstract] [Full Text]
Published Version
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