H3K36 Methylation Regulates Nutrient Stress Response in Saccharomyces cerevisiae by Enforcing Transcriptional Fidelity.
H3K36 Methylation Regulates Nutrient Stress Response in Saccharomyces cerevisiae by Enforcing Transcriptional Fidelity.
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DOI：
10.1016/j.celrep.2017.05.057
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发表时间：
2017-06-13
期刊：
影响因子：
8.8
通讯作者：
Strahl BD
中科院分区：
文献类型：
--
作者：
McDaniel SL;Hepperla AJ;Huang J;Dronamraju R;Adams AT;Kulkarni VG;Davis IJ;Strahl BD
Set2介导的H3K36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（隐藏）转录。虽然Set2抑制隐蔽转录的失败与寿命缩短有关，但隐蔽转录对其他细胞功能的影响程度仍知之甚少。在这里，我们揭示了H3K36甲基化在营养应激反应途径的调节中的作用。我们发现，在SET 2缺失（set2Δ）细胞中，对营养胁迫的转录反应失调，并且与源自基因体内的全基因组双向隐蔽转录相关。从这些隐蔽事件产生的反义转录延伸到它们所产生的基因的启动子中，并且与营养胁迫条件下的有义转录减少相关。这些结果表明，Set2强制转录保真度是诱导和高度调节的转录程序的适当调节的关键。McDaniel等人发现Set2介导的H3K36甲基化对于适当的TOR信号传导和营养应激反应是必需的。缺乏Set2的细胞显示对营养胁迫的破坏的转录响应，其与干扰适当转录的基因内的基因内双向转录增加相关。
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 life span, 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 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. McDaniel et al. find that Set2-mediated H3K36 methylation is necessary for proper TOR signaling and the nutrient stress response. Cells lacking Set2 display a disrupted transcriptional response to nutrient stress that is correlated with increased intragenic bi-directional transcription within genes that interferes with proper transcription.
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影响因子：
8.8
作者：
Huber F;Bunina D;Gupta I;Khmelinskii A;Meurer M;Theer P;Steinmetz LM;Knop M
通讯作者：
Knop M
DOI：
10.1093/bioinformatics/btp527
发表时间：
2009-11-01
期刊：
Bioinformatics (Oxford, England)
影响因子：
--
作者：
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通讯作者：
Daub CO
影响因子：
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作者：
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通讯作者：
Stillman, David J.
影响因子：
5.3
作者：
Fillingham, Jeffrey;Recht, Judith;Greenblatt, Jack F.
通讯作者：
Greenblatt, Jack F.
影响因子：
16
作者：
Joshi, AA;Struhl, K
通讯作者：
Struhl, K