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首页> 外文期刊>Molecular and Cellular Biology >A bipartite operator interacts with a heat shock element to mediate early meiotic induction of Saccharomyces cerevisiae HSP82.
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A bipartite operator interacts with a heat shock element to mediate early meiotic induction of Saccharomyces cerevisiae HSP82.

机译：二分算子与热激元件相互作用，以介导酿酒酵母HSP82的早期减数分裂诱导。

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Although key genetic regulators of early meiotic transcription in Saccharomyces cerevisiae have been well characterized, the activation of meiotic genes is still poorly understood in terms of cis-acting DNA elements and their associated factors. I report here that induction of HSP82 is regulated by the early meiotic IME1-IME2 transcriptional cascade. Vegetative repression and meiotic induction depend on interactions of the promoter-proximal heat shock element (HSE) with a nearby bipartite repression element, composed of the ubiquitous early meiotic motif, URS1 (upstream repression sequence 1), and a novel ancillary repression element. The ancillary repression element is required for efficient vegetative repression, is spatially separable from URS1, and continues to facilitate repression during sporulation. In contrast, URS1 also functions as a vegetative repression element but is converted early in meiosis into an HSE-dependent activation element. An early step in this transformation may be the antagonism of URS1-mediated repression by IME1. The HSE also nonspecifically supports a second major mode of meiotic activation that does not require URS1 but does require expression of IME2 and concurrent starvation. Interestingly, increased rather than decreased URS1-mediated vegetative transcription can be artificially achieved by introducing rare point mutations into URS1 or by deleting the UME6 gene. These lesions offer insight into mechanisms of URS-dependent repression and activation. Experiments suggest that URS1-bound factors functionally modulate heat shock factor during vegetative transcription and early meiotic induction but not during heat shock. The loss of repression and activation observed when the IME2 activation element, T4C, is substituted for the HSE suggests specific requirements for URS1-upstream activation sequence interactions.
机译：尽管酿酒酵母中减数分裂早期转录的关键遗传调控因子已被很好地表征，但就顺式作用DNA元件及其相关因素而言，减数分裂基因的激活仍然知之甚少。我在这里报告说，HSP82的诱导受早期减数分裂IME1-IME2转录级联的调节。营养抑制和减数分裂诱导取决于启动子-近端热休克元件（HSE）与附近的二分抑制元件的相互作用，该元件由普遍存在的早期减数分裂基序URS1（上游抑制序列1）和新型辅助抑制元件组成。辅助抑制元件是有效的植物抑制所必需的，在空间上可与URS1分离，并在孢子形成过程中继续促进抑制。相比之下，URS1也起着植物抑制因子的作用，但在减数分裂早期被转化为HSE依赖性激活因子。此转化的第一步可能是对抗IME1介导的URS1介导的抑制。 HSE还非特异性地支持减数分裂激活的第二种主要模式，该模式不需要URS1，但确实需要IME2的表达和并发饥饿。有趣的是，可以通过将稀有点突变引入URS1或删除UME6基因来人为地增加而不是减少URS1介导的营养转录。这些病变提供了对URS依赖性抑制和激活机制的了解。实验表明，在营养转录和减数分裂早期诱导过程中，URS1结合因子在功能上调节热激因子，但在热激过程中则不起作用。当IME2激活元件T4C代替HSE时，观察到的抑制和激活丧失表明URS1上游激活序列相互作用的特殊要求。

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