The expression of bromodomain-containing proteins that regulate chromatin structure and accessibility must be tightly controlled to ensure the appropriate regulation of gene expression. In the yeast S. cerevisiae, Bromodomain Factor 2 (BDF2) expression is extensively regulated post-transcriptionally during stress by RNase III-mediated decay (RMD), which is triggered by cleavage of the BDF2 mRNA in the nucleus by the RNase III homolog Rnt1p. Previous studies have shown that RMD-mediated down-regulation of BDF2 is hyperactivated in osmotic stress conditions, yet the mechanisms driving the enhanced nuclear cleavage of BDF2 RNA under these conditions remain unknown. Here, we show that RMD hyperactivation can be detected in multiple stress conditions that inhibit mRNA export, and that Rnt1p remains primarily localized in the nucleus during salt stress. We show that globally inhibiting mRNA nuclear export by anchoring away mRNA biogenesis or export factors out of the nucleus can recapitulate RMD hyperactivation in the absence of stress. RMD hyperactivation requires Rnt1p nuclear localization but does not depend on the BDF2 gene endogenous promoter, and its efficiency is affected by the structure of the stem–loop cleaved by Rnt1p. Because multiple stress conditions have been shown to mediate global inhibition of mRNA export, our results suggest that the hyperactivation of RMD is primarily the result of the increased nuclear retention of the BDF2 mRNA during stress.

中文翻译：

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应激诱导的 mRNA 输出抑制触发 RNase III 介导的 BDF2 mRNA 衰变

必须严格控制调节染色质结构和可及性的含溴结构域蛋白的表达，以确保适当调节基因表达。在酿酒酵母中，Bromodomain Factor 2 ( BDF2)表达在压力期间通过 RNase III 介导的衰变 (RMD) 在转录后得到广泛调节，这是由 RNase III 同系物 Rnt1p 在细胞核中切割 BDF2 mRNA 触发的. 先前的研究表明，RMD 介导的BDF2下调在渗透胁迫条件下过度激活，但驱动BDF2增强核裂解的机制这些条件下的 RNA 仍然未知。在这里，我们表明可以在抑制 mRNA 输出的多种胁迫条件下检测到 RMD 过度激活，并且 Rnt1p 在盐胁迫期间主要位于细胞核中。我们表明，通过锚定 mRNA 生物合成或核外输出因子来全局抑制 mRNA 核输出可以在没有压力的情况下重现 RMD 过度激活。RMD 过度激活需要 Rnt1p 核定位但不依赖于BDF2基因内源启动子，其效率受Rnt1p切割的茎环结构的影响。因为多种应激条件已被证明可以介导 mRNA 输出的全局抑制，我们的结果表明 RMD 的过度激活主要是应激期间BDF2 mRNA 核保留增加的结果。