Protein kinase VRK-1 regulates cell invasion and EGL-17/FGF signaling in Caenorhabditis elegans
Protein kinase VRK-1 regulates cell invasion and EGL-17/FGF signaling in Caenorhabditis elegans
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DOI：
10.1016/j.ydbio.2009.08.007
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发表时间：
2009-11-01
影响因子：
2.7
通讯作者：
Askjaer, Peter
中科院分区：
文献类型：
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作者：
Klerkx, Elke P. F.;Alarcon, Pilar;Askjaer, Peter
牛痘相关激酶 (VRK) 在整个动物界中高度保守，可磷酸化多种染色质蛋白和转录因子。在早期秀丽隐杆线虫胚胎中，VRK-1 是正确核膜形成所必需的。在这项工作中，我们通过一种新的线虫 vrk-1 突变等位基因首次研究了 VRK 的发育作用。我们发现 VRK-1 对于雌雄同体的外阴、子宫和子宫的形成以及体细胞性腺和种系的发育和维持至关重要。 VRK-1 在 L3 幼虫阶段通过分隔外阴和体细胞性腺细胞的基底膜调节锚细胞极性和锚细胞入侵的时间。 VRK-1 也是子宫细胞和性成肌细胞的适当规范和增殖所必需的。在 VRK-1 突变体中，成纤维细胞生长因子样蛋白 EGL-17 及其受体 EGL-15 的表达降低，表明 VRK-1 可能至少部分通过激活 FGF 信号传导发挥作用。翻译性 VRK-1::GFP 融合蛋白在腹神经索和外阴前体细胞中的表达可恢复外阴和子宫的形成，表明 VRK-1 具有细胞自主和非自主作用。 (C) 2009 Elsevier Inc. 保留所有权利。
The vaccinia-related kinases (VRKs) are highly conserved throughout the animal kingdom and phosphorylate several chromatin proteins and transcription factors. In early Caenorhabditis elegans embryos, VRK-1 is required for proper nuclear envelope formation. in this work, we present the first investigation of the developmental role of VRKs by means of a novel C elegans vrk-1 mutant allele. We found that VRK-1 is essential in hermaphrodites for formation of the vulva, uterus, and utse and for development and maintenance of the somatic gonad and thus the germ line. VRK-1 regulates anchor cell polarity and the timing of anchor cell invasion through the basement membranes separating vulval and somatic gonadal cells during the L3 larval stage. VRK-1 is also required for proper specification and proliferation of uterine cells and sex myoblasts. Expression of the fibroblast growth factor-like protein EGL-17 and its receptor EGL-15 is reduced in vrk-1 mutants, suggesting that VRK-1 might act at least partially through activation of FGF signaling. Expression of a translational VRK-1::GFP fusion protein in the ventral nerve cord and vulva precursor cells restores vulva and uterus formation, suggesting both cell autonomous and non-autonomous roles of VRK-1. (C) 2009 Elsevier Inc. All rights reserved.