Set2-mediated histone methylation at H3K36 regulates diverse activities, including DNA repair, mRNA splicing, and suppression of inappropriate (cryptic) transcription. Although failure of Set2 to suppress cryptic transcription has been linked to decreased lifespan, the extent to which cryptic transcription influences other cellular functions is poorly understood. Here, we uncover a role for H3K36 methylation in the regulation of the nutrient stress response pathway. We found that the transcriptional response to nutrient stress was dysregulated in SET2-deleted (set2Δ) cells and was correlated with genome-wide bi-directional cryptic transcription that originated from within gene bodies. Antisense transcripts arising from these cryptic events extended into the promoters of the genes from which they arose and were associated with decreased sense transcription under nutrient stress conditions. These results suggest that Set2-enforced transcriptional fidelity is critical to the proper regulation of inducible and highly regulated transcription programs.

译文

H3K36的Set2-mediated组蛋白甲基化调节多种活动,包括DNA修复,mRNA剪接和抑制不适当的 (隐性) 转录。尽管Set2无法抑制隐性转录与寿命缩短有关,但对隐性转录影响其他细胞功能的程度知之甚少。在这里,我们揭示了H3K36甲基化在营养应激反应途径调节中的作用。我们发现,对营养应激的转录反应在SET2-deleted (set2Δ) 细胞中失调,并且与源自基因体内的全基因组双向隐秘转录相关。这些隐秘事件产生的反义转录本延伸到它们产生的基因的启动子中,并且在营养胁迫条件下与有义转录减少有关。这些结果表明,Set2-enforced的转录保真度对于适当调节可诱导和高度调节的转录程序至关重要。

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