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PAR-3是秀丽隐杆线虫远端受精囊上皮细胞极性所必需的。

PAR-3 is required for epithelial cell polarity in the distal spermatheca of C. elegans.

作者信息

Aono Shinya, Legouis Renaud, Hoose Wendy A, Kemphues Kenneth J

机构信息

Department of Molecular Biology and Genetics, Cornell University, 107 Biotechnology Building, Ithaca, NY 14853, USA.

出版信息

Development. 2004 Jun;131(12):2865-74. doi: 10.1242/dev.01146. Epub 2004 May 19.

Abstract

PAR-3 is localized asymmetrically in epithelial cells in a variety of animals from Caenorhabditis elegans to mammals. Although C. elegans PAR-3 is known to act in early blastomeres to polarize the embryo, a role for PAR-3 in epithelial cells of C. elegans has not been established. Using RNA interference to deplete PAR-3 in developing larvae, we discovered a requirement for PAR-3 in spermathecal development. Spermathecal precursor cells are born during larval development and differentiate into an epithelium that forms a tube for the storage of sperm. Eggs must enter the spermatheca to complete ovulation. PAR-3-depleted worms exhibit defects in ovulation. Consistent with this phenotype, PAR-3 is transiently expressed and localized asymmetrically in the developing somatic gonad, including the spermathecal precursor cells of L4 larvae. We found that the defect in ovulation can be partially suppressed by a mutation in IPP-5, an inositol polyphosphate 5-phosphatase, indicating that one effect of PAR-3 depletion is disruption of signaling between oocyte and spermatheca. Microscopy revealed that the distribution of AJM-1, an apical junction marker, and apical microfilaments are severely affected in the distal spermatheca of PAR-3-depleted worms. We propose that PAR-3 activity is required for the proper polarization of spermathecal cells and that defective ovulation results from defective distal spermathecal development.

摘要

从秀丽隐杆线虫到哺乳动物等多种动物的上皮细胞中,PAR-3呈不对称定位。尽管已知秀丽隐杆线虫的PAR-3在早期卵裂球中发挥作用以使胚胎极化,但PAR-3在秀丽隐杆线虫上皮细胞中的作用尚未明确。利用RNA干扰技术在发育中的幼虫中耗尽PAR-3,我们发现了PAR-3在受精囊发育中的必要性。受精囊前体细胞在幼虫发育期间产生,并分化为形成用于储存精子的管道的上皮。卵子必须进入受精囊才能完成排卵。PAR-3耗尽的线虫在排卵方面表现出缺陷。与这种表型一致,PAR-3在发育中的体细胞性腺中短暂表达并呈不对称定位,包括L4幼虫的受精囊前体细胞。我们发现,排卵缺陷可被肌醇多磷酸5-磷酸酶IPP-5的突变部分抑制,这表明PAR-3耗尽的一个影响是破坏卵母细胞与受精囊之间的信号传导。显微镜检查显示,在PAR-3耗尽的线虫的远端受精囊中,顶端连接标记物AJM-1和顶端微丝的分布受到严重影响。我们提出,PAR-3活性是受精囊细胞正确极化所必需的,而排卵缺陷是由远端受精囊发育缺陷导致的。

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