Ahmed Noreen T, Bungard David, Shin Marcus E, Moore Michael, Winter Edward
Thomas Jefferson University, 233 S. 10th St., Philadelphia, PA 19107, USA.
Mol Cell Biol. 2009 Aug;29(16):4352-62. doi: 10.1128/MCB.00305-09. Epub 2009 Jun 15.
Meiotic development in Saccharomyces cerevisiae (sporulation) is controlled by the sequential transcription of temporally distinct sets of meiosis-specific genes. The induction of middle genes controls exit from meiotic prophase, the completion of the nuclear divisions, and spore formation. Middle promoters are controlled through DNA elements termed middle sporulation elements (MSEs) that are bound by the Sum1 repressor during vegetative growth and by the Ndt80 activator during meiosis. It has been proposed that the induction of middle promoters is controlled by competition between Ndt80 and Sum1 for MSE occupancy. Here, we show that the Sum1 repressor can be removed from middle promoters in meiotic cells independent of Ndt80 expression. This process requires the phosphorylation of Sum1 by the meiosis-specific cyclin-dependent kinase-like kinase Ime2. The deletion of HST1, which encodes a Sir2 paralog that interacts with Sum1, bypasses the requirement for this phosphorylation. These findings suggest that in the presence of Ndt80, Sum1 may be displaced from MSEs through a competition-based mechanism but that in the absence of Ndt80, Sum1 is removed from chromatin in a separate pathway requiring the phosphorylation of Sum1 by Ime2 and the inhibition of Hst1.
酿酒酵母中的减数分裂发育（孢子形成）由减数分裂特异性基因的时间上不同的集合的顺序转录控制。中期基因的诱导控制减数分裂前期的退出、核分裂的完成和孢子形成。中期启动子通过称为中期孢子形成元件（MSEs）的DNA元件进行控制，在营养生长期间，MSEs与Sum1阻遏物结合，而在减数分裂期间与Ndt80激活剂结合。有人提出，中期启动子的诱导由Ndt80和Sum1之间对MSE占据的竞争控制。在这里，我们表明，减数分裂细胞中的中期启动子上的Sum1阻遏物可以独立于Ndt80表达而被去除。这个过程需要减数分裂特异性细胞周期蛋白依赖性激酶样激酶Ime2对Sum1进行磷酸化。编码与Sum1相互作用的Sir2旁系同源物的HST1的缺失绕过了这种磷酸化的需求。这些发现表明，在存在Ndt80的情况下，Sum1可能通过基于竞争的机制从MSEs上被取代，但在不存在Ndt80的情况下，Sum1通过一个单独的途径从染色质上被去除，该途径需要Ime2对Sum1进行磷酸化并抑制Hst1。
