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秀丽隐杆线虫不对称细胞分裂过程中前部细胞特异性mec-3表达的调控

Regulation of anterior cell-specific mec-3 expression during asymmetric cell division in C. elegans.

作者信息

Way J C, Run J Q, Wang A Y

机构信息

Department of Biology, Rutgers University, Piscataway, New Jersey 08855.

出版信息

Dev Dyn. 1992 Aug;194(4):289-302. doi: 10.1002/aja.1001940405.

Abstract

The homeobox-containing mec-3 gene of C. elegans is expressed in 10 mechanosensory neurons and is necessary for these cells to acquire their fate. All the mec-3-expressing cells are anterior daughters from an asymmetric cell division. In this paper, we examine the expression of a mec-3--lacZ fusion in the presence of mutations that may disrupt asymmetric cell division or anterior-posterior positional information, as well as mutations that may specifically alter mec-3 expression. A mutation in lin-17 causes production of additional mec-3-expressing cells and can have its effect on the cell division that produces a mec-3-expressing cell. In a lin-5 mutant, in which postembryonic blast cells do not complete cell division and become polyploid, blast cells that would give rise to mec-3-expressing daughters instead express mec-3 themselves. In a lin-12 glp-1 double mutant, which is disrupted for many cell interactions in which two cells compete for the same fate, mec-3 expression is unaffected. These results are consistent with a model for asymmetric cell division in which the mec-3-expressing cell and its sister are different immediately upon cell division, rather than acquiring differences through later interaction with each other or their surroundings. lin-17 mutant animals also show defects in the position of the PVM cell and the PLM axons. Animals mutant in unc-73 and unc-40, known to have axon outgrowth defects, also show errors in PVM position and a low frequency of additional mec-3-expressing cells, as well as occasional secondary vulval protrusions, a common phenotype of lin-17 animals. Many other mutations have either no effect on mec-3 expression or an effect that can be largely predicted from previously known phenotypes: these include mab-5, mig-1, unc-53, egl-5, lin-32, and egl-27. unc-11 shows an unexpected and specific defect in mec-3 expression in the PVD neurons, but not in the other mec-3-expressing cells. Two mutations that suppress the egg-laying defect of unc-86 have no effect on the mec-3 expression defect in an unc-86 mutant.

摘要

秀丽隐杆线虫中含有同源异型框的mec-3基因在10个机械感觉神经元中表达,对于这些细胞获得其命运而言是必需的。所有表达mec-3的细胞都是不对称细胞分裂产生的前侧子代细胞。在本文中,我们研究了在可能破坏不对称细胞分裂或前后位置信息的突变存在的情况下,以及可能特异性改变mec-3表达的突变存在的情况下,mec-3与lacZ的融合蛋白的表达情况。lin-17中的一个突变导致产生额外的表达mec-3的细胞,并且其作用可能发生在产生表达mec-3的细胞的细胞分裂过程中。在lin-5突变体中,胚胎后胚细胞不能完成细胞分裂并变成多倍体,原本会产生表达mec-3的子代细胞的胚细胞自身反而表达mec-3。在lin-12 glp-1双突变体中,许多细胞间相互作用被破坏,其中两个细胞竞争相同的命运,但mec-3的表达未受影响。这些结果与不对称细胞分裂的模型一致,即表达mec-3的细胞及其姐妹细胞在细胞分裂后立即不同,而不是通过后来彼此或与周围环境的相互作用获得差异。lin-17突变动物在PVM细胞和PLM轴突的位置上也表现出缺陷。已知在unc-73和unc-40中发生突变的动物存在轴突生长缺陷,它们在PVM位置上也出现错误,并且产生额外的表达mec-3的细胞的频率较低,以及偶尔出现继发性外阴突出,这是lin-17动物的常见表型。许多其他突变要么对mec-3的表达没有影响,要么其影响可以根据先前已知的表型大致预测:这些突变包括mab-5、mig-1、unc-53、egl-5、lin-32和egl-27。unc-11在PVD神经元的mec-3表达中表现出意想不到的特异性缺陷,但在其他表达mec-3的细胞中没有。两个抑制unc-86产卵缺陷的突变对unc-86突变体中的mec-3表达缺陷没有影响。

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