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2 Publications

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    Rubin Lab
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    12/29/95 | Drosophila homologs of baculovirus inhibitor of apoptosis proteins function to block cell death.
    Hay BA, Wassarman DA, Rubin GM
    Cell. 1995 Dec 29;83(7):1253-62. doi: 10.1186/gb-2007-8-7-r145

    Apoptotic cell death is a mechanism by which organisms eliminate superfluous or harmful cells. Expression of the cell death regulatory protein REAPER (RPR) in the developing Drosophila eye results in a small eye owing to excess cell death. We show that mutations in thread (th) are dominant enhancers of RPR-induced cell death and that th encodes a protein homologous to baculovirus inhibitors of apoptosis (IAPs), which we call Drosophila IAP1 (DIAP1). Overexpression of DIAP1 or a related protein, DIAP2, in the eye suppresses normally occurring cell death as well as death due to overexpression of rpr or head involution defective. IAP death-preventing activity localizes to the N-terminal baculovirus IAP repeats, a motif found in both viral and cellular proteins associated with death prevention.

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    Rubin Lab
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    06/16/95 | Yan functions as a general inhibitor of differentiation and is negatively regulated by activation of the Ras1/MAPK pathway.
    Rebay I, Rubin GM
    Cell. 1995 Jun 16;81(6):857-66. doi: 10.1186/gb-2007-8-7-r145

    Drosophila yan has been postulated to act as an antagonist of the proneural signal mediated by the sevenless/Ras1/MAPK pathway. We have mutagenized the eight MAPK phosphorylation consensus sites of yan and examined the effects of overexpressing the mutant protein in transgenic flies and transfected S2 cultured cells. Our results suggest that phosphorylation by MAPK affects the stability and subcellular localization of yan, resulting in rapid down-regulation of yan activity. Furthermore, MAPK-mediated down-regulation of yan function appears to be critical for the proper differentiation of both neuronal and nonneuronal tissues throughout development, suggesting that yan is an essential component of a general timing mechanism controlling the competence of a cell to respond to inductive signals.

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