Mother and Daughter Are Doing Fine: Asymmetric Cell Division in Yeast

Unlike other SWI5-dependent transcripts, which are transcribed as cells exit mitosis, activation of HO expression is delayed until the late G1 phase of the next cell cycle. Thus, temporal as well as spatial regulation might be important for restricting HO expression to mother cells. Sil and Herskowitz 1996xSil, A and Herskowitz, I. Cell. 1996; 84Abstract | Full Text | Full Text PDF | PubMed | Scopus (183)See all ReferencesSil and Herskowitz 1996 and Bobola et al. 1996xBobola, N, Jansen, R.-P, Shin, T.-H, and Nasmyth, K. Cell. 1996; 84Abstract | Full Text | Full Text PDF | PubMed | Scopus (262)See all ReferencesBobola et al. 1996 propose a model that incorporates both notions: as cells exit mitosis, Swi5p enters the nucleus of both mother and daughter cells, where it activates transcription of ASH1. Asymmetric accumulation of Ash1p in the daughter cell nucleus brought about by She proteins therefore coincides with entry of Swi5p into the nucleus (compare Figure AFigure A and Figure BFigure B). In daughter cells, Ash1p inhibits Swi5p function or interferes with activation of HO transcription (both possibilities are indicated by a question mark in Figure 3Figure 3). Although Ash1p is absent in mother cells, Swi5p cannot activate HO transcription because it must await Swi4p and Swi6p function, which confines HO transcription to the late G1 phase of the cell cycle. This temporal delay in activation of HO employed by Swi4p and Swi6p might provide a time window in which Ash1p can accumulate in the daughter cell nucleus to levels sufficient to inhibit all Swi5p function or to prevent binding of transcriptional activators to the HO promoter (Sil and Herskowitz 1996xSil, A and Herskowitz, I. Cell. 1996; 84Abstract | Full Text | Full Text PDF | PubMed | Scopus (183)See all ReferencesSil and Herskowitz 1996). This could lead to repression of HO expression in daughter cells (Figure 3Figure 3).Figure 3A Model for Differential Regulation of HO Gene Expression in Mother and Daughter CellsAccumulation of Ash1p in the daughter cell nucleus coincides with the entry of Swi5p into the nucleus in mother (M) and daughter (D) cells. Ash1p either inhibits Swi5p function or interferes with activation of HO transcription (both possibilities are indicated by question marks) in daughter cells. In mother cells, Ash1p is absent, but Swi5p is not sufficient to activate HO transcription. Swi4p and Swi6p, which form a complex, delay HO transcription to the late G1 phase of the cell cycle. This delay might provide a time window for Ash1p to inactivate the HO promoter in daughter cells.View Large Image | View Hi-Res Image | Download PowerPoint SlideIn 1979, StrathernxStrathern, J.N and Herskowitz, I. Cell. 1979; 17: 371–381Abstract | Full Text PDF | PubMed | Scopus (112)See all References1979, Strathern and Herskowitz showed that mother and daughter cells differ in their competence to switch mating type. The first breakthrough in understanding mother–daughter specificity of mating-type switching was the finding that the HO gene is expressed only in mother cells (Nasmyth 1983xNasmyth, K. Nature. 1983; 302: 670–676Crossref | PubMed | Scopus (138)See all ReferencesNasmyth 1983). Now, the identification of a daughter cell–specific repressor of HO expression might well have solved the puzzle of how HO expression, and thus mating-type switching, is confined to mother cells. It seems, however, that ASH1 is not all that different from HO: it too accumulates preferentially in one of the two descendent cells—this time in the daughter cells. Although the origin of this asymmetry is not understood in detail, actin-dependent transport may be responsible. In the Drosophila oocyte, polarized microtubules and the actin cytoskeleton are thought to provide a structural basis for localizing cell fate determinants (reviewed byLehmann 1995xLehmann, R. Cell. 1995; 83: 353–356Abstract | Full Text PDF | PubMed | Scopus (39)See all ReferencesLehmann 1995; Erdelyi et al. 1995xErdelyi, M, Michon, A.-M, Guichet, A, Glotzer, J.B, and Ephrussi, A. Nature. 1995; 377: 524–527Crossref | PubMedSee all ReferencesErdelyi et al. 1995). Perhaps the polarized actin cytoskeleton plays a similar role in facilitating localization of Ash1p. Utilizing cytoskeletal asymmetry to generate developmental asymmetry may prove to be a common mechanism by which a cell generates two daughter cells of different fates.