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拉赫西斯依赖的卵母细胞信号调控雌性配子体细胞的发育。

LACHESIS-dependent egg-cell signaling regulates the development of female gametophytic cells.

机构信息

Center for Plant Molecular Biology (ZMBP), University of Tübingen, Tübingen, Germany.

出版信息

Development. 2012 Feb;139(3):498-502. doi: 10.1242/dev.075234. Epub 2011 Dec 21.

Abstract

In contrast to animals, plant germ cells are formed along with accessory cells in specialized haploid generations, termed gametophytes. The female gametophyte of flowering plants consists of four different cell types, which exert distinct functions in the reproductive process. For successful fertilization, the development of the four cell types has to be tightly coordinated; however, the underlying mechanisms are not yet understood. We have previously isolated the lachesis (lis) mutant, which forms supernumerary gametes at the expense of adjacent accessory cells. LIS codes for the Arabidopsis homolog of the pre-mRNA splicing factor PRP4 and shows a dynamic expression pattern in the maturing female gametophyte. Here, we used LIS as a molecular tool to study cell-cell communication in the female gametophyte. We show that reducing LIS transcript amounts specifically in the egg cell, affects the development of all female gametophytic cells, indicating that cell differentiation in the female gametophyte is orchestrated by the egg cell. Among the defects observed is the failure of homotypic nuclei fusion in the central cell and, as a consequence, a block in endosperm formation. LIS-mediated egg cell signaling, thus, provides a safeguard mechanism that prevents the formation of nurturing tissue in the absence of a functional egg cell.

摘要

与动物不同,植物的生殖细胞是在专门的单倍体世代中与辅助细胞一起形成的,称为配子体。开花植物的雌性配子体由四种不同的细胞类型组成,它们在生殖过程中发挥着不同的功能。为了成功受精,四种细胞类型的发育必须紧密协调;然而,其潜在机制尚不清楚。我们之前分离了 lachesis(lis)突变体,该突变体以牺牲相邻的辅助细胞为代价形成多余的配子。LIS 编码拟南芥前体 mRNA 剪接因子 PRP4 的同源物,在成熟的雌性配子体中表现出动态的表达模式。在这里,我们将 LIS 用作研究雌性配子体中细胞间通讯的分子工具。我们表明,特异性减少卵母细胞中的 LIS 转录本数量会影响所有雌性配子体细胞的发育,这表明雌性配子体中的细胞分化是由卵母细胞协调的。观察到的缺陷之一是中央细胞中同源核融合的失败,以及随之而来的胚乳形成受阻。因此,LIS 介导的卵母细胞信号转导提供了一种保护机制,防止在没有功能卵母细胞的情况下形成营养组织。

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