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Regulation and function of the LIN-31 WH and LIN-1 Ets transcription factors during Caenorhabditis elegans vulval induction
Regulation and function of the LIN-31 WH and LIN-1 Ets transcription factors during Caenorhabditis elegans vulval induction
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Regulation and function of the LIN-31 WH and LIN-1 Ets transcription factors during Caenorhabditis elegans vulval induction
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Regulation and function of the LIN-31 WH and LIN-1 Ets transcription factors during Caenorhabditis elegans vulval induction
Regulation and function of the LIN-31 WH and LIN-1 Ets transcription factors during Caenorhabditis elegans vulval induction

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Regulation and function of the LIN-31 WH and LIN-1 Ets transcription factors during Caenorhabditis elegans vulval induction
Regulation and function of the LIN-31 WH and LIN-1 Ets transcription factors during Caenorhabditis elegans vulval induction
Dissertation

Regulation and function of the LIN-31 WH and LIN-1 Ets transcription factors during Caenorhabditis elegans vulval induction

1999
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Overview
The let-23 Receptor/let-60 Ras/mpk-1 MAP kinase signaling pathway induces the formation of the vulva in C. elegans. We show that the lin-31 and lin-1 transcription factors act downstream of mpk-1 MAP kinase. Both proteins can be phosphorylated by MAP kinase in vitro and in vivo. A phophorylation-defective version of LIN-31 blocks vulval induction, and a LIN-31::VP16 chimeric activator promotes vulval induction, suggesting that LIN-31 may act as a transcriptional activator when phosphorylated. LIN-31 WH and LIN-1 Ets also physically associate, and this association is blocked by MAP kinase phosphorylation of LIN-31. Vulval induction is blocked when LIN-1/LIN-31 dissociation is prevented. We also show that LIN-31 only responds to MAP kinase in the vulva, and not in other tissues where MAP kinase is known to function. lin-31 is necessary for the expression of a vulval-specific marker, and ectopic expression of lin-31 is sufficient to induce expression of this marker in another let-23 Receptor-responsive cell type. These results suggest that LIN-31 may act as a tissue-specific effector of the let-23 Receptor/let-60 Ras/mpk-1 MAP kinase signaling pathway, and may contribute to the expression of the vulval-specific response. Little is also known about how the vulval precursor cells acquire their specific developmental competence. We found that lin-31 is down-regulated in P5.p, P6.p, and P7.p, just before these cells divide to generate vulval tissue. Activation of the let-23 Receptor/ let-60 Ras/mpk-1 MAP kinase signaling pathway is both necessary and sufficient for down-regulation of lin-31 in these cells. This down-regulation of LIN-31 is physiologically important for vulval development, as ectopic LIN-31 expression results in the formation of defective vulvae. Through the use of promoter deletions and a transgenic animal assay, a number of cis-acting elements that contribute to lin-31 expression were identified.
Publisher
ProQuest Dissertations & Theses
ISBN
9780599240735, 0599240733