Regulation of spindle pole function by an intermediary metabolite.

Regulation of spindle pole function by an intermediary metabolite.
复制标题

中间代谢物对纺锤体极功能的调节。

DOI:
10.1091/mbc.e04-02-0128
复制
发表时间:
2004
影响因子:
3.3
通讯作者:
Neiman,AaronM
Neiman,AaronM
中科院分区:
生物学3区
文献类型:
--
作者:
Nickas,MarkE;Diamond,AvivaE;Yang,Min-Jay;Neiman,AaronM

文献摘要

相似文献

酵母(酿酒酵母)的孢子形成依赖于减数分裂II开始时纺锤极体(SPBs)的修饰,使它们能够促进新膜的形成。在孢子形成过程中,环境碳源的消耗导致每个减数分裂II纺锤体仅修饰一个SPB,形成一个双孢子子囊,称为非姐妹二体(NSD)。我们发现,当乙酸为主要碳源时,在乙酸转化为葡萄糖所需的乙醛酸途径受损的突变体产生非甾体激酶。当碳源为甘油时,野生型细胞产生非甾体抗裂肽,甘油独立于乙醛酸途径转化为葡萄糖。在甘油中NSD形成过程中,只有减数分裂I/II转变时产生的两个spb(“子”)被修饰。在这些条件下,SPB组分Mpc70p和Spo74p不被募集到母SPB。此外,Mpc70p和Spo74p的过表达抑制了甘油中NSD的形成。我们的研究结果表明,产孢过程中乙醛酸途径的通量通过Mpc70p和Spo74p的募集来调节母spb的修饰。这些结果定义了一种细胞反应,其中中间代谢物的积累作为调节子细胞形成数量的生物合成能力的衡量标准。
Spore formation in the yeastSaccharomyces cerevisiaedepends on a modification of spindle pole bodies (SPBs) at the onset of meiosis II that allows them to promote de novo membrane formation. Depletion of the environmental carbon source during sporulation results in modification of only one SPB from each meiosis II spindle and formation of a two-spored ascus, called a nonsister dyad (NSD). We have found that mutants impaired in the glyoxylate pathway, which is required for the conversion of acetate to glucose, make NSDs when acetate is the primary carbon source. Wild-type cells make NSDs when the carbon source is glycerol, which is converted to glucose independently of the glyoxylate pathway. During NSD formation in glycerol, only the two SPBs created at the meiosis I/II transition (“daughters”) are modified. In these conditions, the SPB components Mpc70p and Spo74p are not recruited to mother SPBs. Moreover, cooverexpression of Mpc70p and Spo74p suppresses NSD formation in glycerol. Our findings indicate that flux through the glyoxylate pathway during sporulation regulates modification of mother SPBs via recruitment of Mpc70p and Spo74p. These results define a cellular response in which the accumulation of an intermediary metabolite serves as a measure of biosynthetic capacity to regulate the number of daughter cells formed.