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Disruption of Caenorhabditis elegans muscle structure and function caused by mutation of troponin I.肌钙蛋白I突变导致秀丽隐杆线虫肌肉结构和功能的破坏。
Biophys J. 2004 Feb;86(2):991-1001. doi: 10.1016/S0006-3495(04)74174-0.
2
Regulation of actin filament dynamics by actin depolymerizing factor/cofilin and actin-interacting protein 1: new blades for twisted filaments.肌动蛋白解聚因子/丝切蛋白和肌动蛋白相互作用蛋白1对肌动蛋白丝动力学的调节:扭曲丝的新刀片
Biochemistry. 2003 Nov 25;42(46):13363-70. doi: 10.1021/bi034600x.
3
Actin assembly and endocytosis: from yeast to mammals.肌动蛋白组装与内吞作用:从酵母到哺乳动物
Annu Rev Cell Dev Biol. 2003;19:287-332. doi: 10.1146/annurev.cellbio.19.111401.093127.
4
Talin loss-of-function uncovers roles in cell contractility and migration in C. elegans.塔林功能丧失揭示了其在秀丽隐杆线虫细胞收缩性和迁移中的作用。
J Cell Sci. 2003 Oct 1;116(Pt 19):3871-8. doi: 10.1242/jcs.00705. Epub 2003 Aug 12.
5
Specific requirement for two ADF/cofilin isoforms in distinct actin-dependent processes in Caenorhabditis elegans.秀丽隐杆线虫中两种肌动蛋白解聚因子/丝切蛋白亚型在不同肌动蛋白依赖性过程中的特定要求。
J Cell Sci. 2003 May 15;116(Pt 10):2073-85. doi: 10.1242/jcs.00421. Epub 2003 Apr 1.
6
An Eph receptor sperm-sensing control mechanism for oocyte meiotic maturation in Caenorhabditis elegans.秀丽隐杆线虫中一种用于卵母细胞减数分裂成熟的Eph受体精子感应控制机制。
Genes Dev. 2003 Jan 15;17(2):187-200. doi: 10.1101/gad.1028303.
7
Systematic functional analysis of the Caenorhabditis elegans genome using RNAi.利用RNA干扰对线虫基因组进行系统功能分析。
Nature. 2003 Jan 16;421(6920):231-7. doi: 10.1038/nature01278.
8
Actin dynamics: tropomyosin provides stability.肌动蛋白动力学:原肌球蛋白提供稳定性。
Curr Biol. 2002 Aug 6;12(15):R523-5. doi: 10.1016/s0960-9822(02)01028-x.
9
Caenorhabditis elegans inositol 5-phosphatase homolog negatively regulates inositol 1,4,5-triphosphate signaling in ovulation.秀丽隐杆线虫肌醇5-磷酸酶同源物在排卵过程中负向调节肌醇1,4,5-三磷酸信号传导。
Mol Biol Cell. 2002 May;13(5):1641-51. doi: 10.1091/mbc.02-01-0008.
10
Tropomyosin inhibits ADF/cofilin-dependent actin filament dynamics.原肌球蛋白抑制ADF/丝切蛋白依赖的肌动蛋白丝动力学。
J Cell Biol. 2002 Mar 18;156(6):1065-76. doi: 10.1083/jcb.200110013.

原肌球蛋白和肌钙蛋白是秀丽隐杆线虫生殖系统中卵巢收缩所必需的。

Tropomyosin and troponin are required for ovarian contraction in the Caenorhabditis elegans reproductive system.

作者信息

Ono Kanako, Ono Shoichiro

机构信息

Department of Pathology, Emory University, Atlanta, Georgia 30322, USA.

出版信息

Mol Biol Cell. 2004 Jun;15(6):2782-93. doi: 10.1091/mbc.e04-03-0179. Epub 2004 Apr 2.

DOI:10.1091/mbc.e04-03-0179
PMID:15064356
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC420102/
Abstract

Ovulation in the nematode Caenorhabditis elegans is coordinated by interactions between the somatic gonad and germ cells. Myoepithelial sheath cells of the proximal ovary are smooth muscle-like cells, but the regulatory mechanism of their contraction is unknown. We show that contraction of the ovarian muscle requires tropomyosin and troponin, which are generally major actin-linked regulators of contraction of striated muscle. RNA interference of tropomyosin or troponin C caused sterility by inhibiting ovarian contraction that is required for expelling mature oocytes into the spermatheca where fertilization takes place, thus causing accumulation of endomitotic oocytes in the ovary. Tropomyosin and troponin C were associated with actin filaments in the myoepithelial sheath, and the association of troponin C with actin was dependent on tropomyosin. A mutation in the actin depolymerizing factor/cofilin gene suppressed the ovulation defects by RNA interference of tropomyosin or troponin C. These results strongly suggest that tropomyosin and troponin are the actin-linked regulators for contraction of ovarian muscle in the C. elegans reproductive system.

摘要

线虫秀丽隐杆线虫的排卵是由体细胞性腺和生殖细胞之间的相互作用协调的。近端卵巢的肌上皮鞘细胞是平滑肌样细胞,但其收缩的调节机制尚不清楚。我们发现卵巢肌肉的收缩需要原肌球蛋白和肌钙蛋白,它们通常是横纹肌收缩的主要肌动蛋白连接调节因子。对原肌球蛋白或肌钙蛋白C进行RNA干扰会抑制卵巢收缩,从而导致不育,而卵巢收缩是将成熟卵母细胞排入受精发生的受精囊所必需的,进而导致卵巢中多线期卵母细胞的积累。原肌球蛋白和肌钙蛋白C与肌上皮鞘中的肌动蛋白丝相关,并且肌钙蛋白C与肌动蛋白的结合依赖于原肌球蛋白。肌动蛋白解聚因子/丝切蛋白基因的突变通过对原肌球蛋白或肌钙蛋白C进行RNA干扰来抑制排卵缺陷。这些结果有力地表明,原肌球蛋白和肌钙蛋白是秀丽隐杆线虫生殖系统中卵巢肌肉收缩的肌动蛋白连接调节因子。