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DNA损伤调节TOR激酶与RNA聚合酶II转录基因的直接关联。

DNA damage regulates direct association of TOR kinase with the RNA polymerase II-transcribed gene.

作者信息

Panday Arvind, Gupta Ashish, Srinivasa Kavitha, Xiao Lijuan, Smith Mathew D, Grove Anne

机构信息

Department of Biological Sciences, Louisiana State University, Baton Rouge, LA 70803.

Department of Biological Sciences, Louisiana State University, Baton Rouge, LA 70803

出版信息

Mol Biol Cell. 2017 Sep 1;28(18):2449-2459. doi: 10.1091/mbc.E17-01-0024. Epub 2017 Jul 12.

DOI:10.1091/mbc.E17-01-0024
PMID:28701348
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5576907/
Abstract

The mechanistic target of rapamycin complex 1 (mTORC1) senses nutrient sufficiency and cellular stress. When mTORC1 is inhibited, protein synthesis is reduced in an intricate process that includes a concerted down-regulation of genes encoding rRNA and ribosomal proteins. The high-mobility group protein Hmo1p has been implicated in coordinating this response to mTORC1 inhibition. We show here that Tor1p binds directly to the gene (but not to genes that are not linked to ribosome biogenesis) and that the presence of Tor1p is associated with activation of gene activity. Persistent induction of DNA double-strand breaks or mTORC1 inhibition by rapamycin results in reduced levels of mRNA, but only in the presence of Tor1p. This down-regulation is accompanied by eviction of Ifh1p and recruitment of Crf1p, followed by concerted dissociation of Hmo1p and Tor1p. These findings uncover a novel role for TOR kinase in control of gene activity by direct association with an RNA polymerase II-transcribed gene.

摘要

雷帕霉素复合物1（mTORC1）的作用机制靶点可感知营养充足和细胞应激。当mTORC1受到抑制时，蛋白质合成会在一个复杂的过程中减少，该过程包括对编码rRNA和核糖体蛋白的基因进行协同下调。高迁移率族蛋白Hmo1p参与协调对mTORC1抑制的这种反应。我们在此表明，Tor1p直接与该基因结合（但不与不与核糖体生物合成相关的基因结合），并且Tor1p的存在与基因活性的激活相关。持续诱导DNA双链断裂或用雷帕霉素抑制mTORC1会导致mRNA水平降低，但仅在存在Tor1p的情况下。这种下调伴随着Ifh1p的逐出和Crf1p的募集，随后是Hmo1p和Tor1p的协同解离。这些发现揭示了TOR激酶通过与RNA聚合酶II转录的基因直接结合来控制基因活性的新作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6b75/5576907/c265dcd40b48/2449fig15.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6b75/5576907/8dfd4a80a8b1/2449fig1.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6b75/5576907/d45ed9239788/2449fig11.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6b75/5576907/c265dcd40b48/2449fig15.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6b75/5576907/8dfd4a80a8b1/2449fig1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6b75/5576907/5957fded70c6/2449fig2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6b75/5576907/db0b2df48adf/2449fig3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6b75/5576907/5e2f162f4fba/2449fig4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6b75/5576907/99289e35babe/2449fig5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6b75/5576907/56e1c670f4ec/2449fig6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6b75/5576907/dd0a7da0ca16/2449fig7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6b75/5576907/eaf3b4f13c0e/2449fig8.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6b75/5576907/c4b18d3c8ef2/2449fig9.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6b75/5576907/a6501c0ea7f4/2449fig10.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6b75/5576907/d45ed9239788/2449fig11.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6b75/5576907/199296050e0e/2449fig12.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6b75/5576907/22e43fb6aa33/2449fig13.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6b75/5576907/bc6c59d9ed36/2449fig14.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6b75/5576907/c265dcd40b48/2449fig15.jpg

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