Linking asymmetric division to cell fate: teaching an old microbe new tricks
Linking asymmetric division to cell fate: teaching an old microbe new tricks
复制标题
DOI：
10.1101/gad.13.4.377
复制
发表时间：
1999-02-15
影响因子：
10.5
通讯作者：
Dworkin, J
中科院分区：
文献类型：
--
作者：
Losick, R;Dworkin, J
Understanding the connection between cell division and cell fate is a fundamental challenge in developmental biology. In organisms ranging from microbes to mammals, cell division can give rise to progeny cells that differ in fate from one another. In some cases, cell specificity is imposed by external cues that differentially influence the fate of the progeny cells. In other cases, specificity is established by an intrinsic asymmetry in the progenitor cell (Horvitz and Herskowitz 1992). In such cases, cell specificity is frequently attributed to the preferential segregation of a cell-fate determinant to one progeny cell. Thus, in Drosophila melanogaster, the cellfate determinants Numb and Prospero differentially localize to the basal side of the dividing neuroblast, with Prospero doing so in a manner that depends on the localization of another protein (Miranda) to the basal cortex (Hawkins and Garriga 1998). Likewise, in the budding yeast Saccharomyces cerevisiae, the distinct fate of the newborn cell (an inability to undergo a switch in mating type) is determined by the transport into the bud prior to cytokinesis of the mRNA for a repressor protein (ASH1p) that prevents mating type switching (Long et al. 1997; Takizawa et al. 1997). The subject of this review is Bacillus subtilis, a spore-forming bacterium in which a visibly asymmetric process of cell division gives rise to progeny cells that differ in fate from one another as well as from the progenitor cell. Here too, as we shall see, the subcellular distribution of a cell-fate determinant (a serine phosphatase known as SpoIIE) is involved in the establishment of cell fate. As reported in this issue, Frandsen et al.(1999) have, however, cleverly taught B. subtilis the trick of sporulating in a manner that bypasses the SpoIIE determinant. Taking advantage of an idiosyncratic feature of chromosome segregation during asymmetric division, these workers have devised a mechanism of cell specification that is dictated by the asymmetric distribution of a gene, rather than the localization of a protein.
