kin-18, a C-elegans protein kinase involved in feeding
kin-18, a C-elegans protein kinase involved in feeding
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DOI：
10.1016/s0378-1119(01)00752-1
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发表时间：
2001-11-28
期刊：
影响因子：
3.5
通讯作者：
Cobb, MH
中科院分区：
文献类型：
--
作者：
Berman, KS;Hutchison, M;Cobb, MH
TAO1和TAO2是最近被描述的蛋白激酶，它们的初步特征使它们处于应激反应MAPK通路的丝裂原活化蛋白激酶(MAPK)/细胞外信号调节激酶(ERK)激酶(MEKK)水平。由于它们的生理作用尚未确定，我们试图研究它们的线虫同源基因，以了解更多关于它们的功能。在线虫中，KIN-18编码一种未知蛋白，其催化结构域与TAO1和TAO2有60%以上的同源性。我们证明KIN-18是一个120 kDa的蛋白，它的启动子在线虫的咽部和肠道中很活跃。为了进一步了解TAO/KIN-18的功能，我们研究了组成活性形式的TAO1或KIN-18的表达如何影响完整蠕虫的生理。表达活性形式的TAO1或KIN-18的线虫菌株通过咽电图测得咽电生理学改变。这些蠕虫生长更慢，产卵更少，这些表型可能是由于摄食量减少造成的。我们还发现了一个线虫基因，它编码一种与哺乳动物MAPK/ERK Kinase(MEK)4类似的蛋白激酶，其启动子在咽部活跃。它在体外被TAO1磷酸化，并与TAO1发生物理作用。(C)2001 Elsevier Science B.V.保留所有权利。
TAO1 and TAO2 are recently described protein kinases whose initial characterization has placed them at the mitogen-activated protein kinase (MAPK)/extracellular signal-regulated kinase (ERK) kinase kinase (MEKK) level of stress-responsive MAPK pathways. Because their physiological roles have not been identified, we sought to study their C elegans homolog to learn more about their functions. kin-18 encodes a previously uncharacterized protein in C. elegans whose catalytic domain shares over 60% identity with TAO1 and TAO2. We demonstrate that KIN-18 is a protein of 120 kDa whose promoter is active in the pharynx and intestine of C. elegans. To learn more about TAO/KIN-18 function, we studied how expression of constitutively active forms of TAO1 or KIN-18 would affect the physiology of intact worms. Strains Of C elegans expressing active forms of TAO1 or KIN-18 exhibit altered pharyngeal electrophysiology as measured by electropharyngeogram. These worms grow more slowly and lay fewer eggs, phenotypes that could result from reduced feeding. We have also identified a C elegans gene that encodes a protein kinase similar to mammalian MAPK/ERK Kinase (MEK) 4 whose promoter is active in the pharynx. It is phosphorylated by TAO1 in vitro and physically interacts with TAO1. (C) 2001 Elsevier Science B.V. All rights reserved.