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在秀丽隐杆线虫的阴门发育过程中,β-连环蛋白同源物BAR-1和LET-60 Ras协同调节Hox基因lin-39。

The beta-catenin homolog BAR-1 and LET-60 Ras coordinately regulate the Hox gene lin-39 during Caenorhabditis elegans vulval development.

作者信息

Eisenmann D M, Maloof J N, Simske J S, Kenyon C, Kim S K

机构信息

Department of Developmental Biology, Stanford University, Stanford, CA 94305, USA.

出版信息

Development. 1998 Sep;125(18):3667-80. doi: 10.1242/dev.125.18.3667.

Abstract

In C. elegans, the epithelial Pn.p cells adopt either a vulval precursor cell fate or fuse with the surrounding hypodermis (the F fate). Our results suggest that a Wnt signal transduced through a pathway involving the beta-catenin homolog BAR-1 controls whether P3.p through P8.p adopt the vulval precursor cell fate. In bar-1 mutants, P3.p through P8.p can adopt F fates instead of vulval precursor cell fates. The Wnt/bar-1 signaling pathway acts by regulating the expression of the Hox gene lin-39, since bar-1 is required for LIN-39 expression and forced lin-39 expression rescues the bar-1 mutant phenotype. LIN-39 activity is also regulated by the anchor cell signal/let-23 receptor tyrosine kinase/let-60 Ras signaling pathway. Our genetic and molecular experiments show that the vulval precursor cells can integrate the input from the BAR-1 and LET-60 Ras signaling pathways by coordinately regulating activity of the common target LIN-39 Hox.

摘要

在秀丽隐杆线虫中,上皮Pn.p细胞要么采用外阴前体细胞命运,要么与周围的皮下组织融合(F命运)。我们的结果表明,通过涉及β-连环蛋白同源物BAR-1的途径转导的Wnt信号控制P3.p至P8.p是否采用外阴前体细胞命运。在bar-1突变体中,P3.p至P8.p可以采用F命运而不是外阴前体细胞命运。Wnt/bar-1信号通路通过调节Hox基因lin-39的表达发挥作用,因为bar-1是LIN-39表达所必需的,而强制表达lin-39可挽救bar-1突变体表型。LIN-39活性也受锚定细胞信号/let-23受体酪氨酸激酶/let-60 Ras信号通路的调节。我们的遗传和分子实验表明,外阴前体细胞可以通过协调调节共同靶标LIN-39 Hox的活性来整合来自BAR-1和LET-60 Ras信号通路的输入。

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