Elucidating the regulatory mechanism of Swi1 prion in global transcription and stress responses.
Elucidating the regulatory mechanism of Swi1 prion in global transcription and stress responses.
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DOI:
10.1038/s41598-020-77993-0
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发表时间:
2020-12-14
影响因子:
4.6
通讯作者:
Li L
中科院分区:
文献类型:
--
作者:
Du Z;Regan J;Bartom E;Wu WS;Zhang L;Goncharoff DK;Li L
Transcriptional regulators are prevalent among identified prions in Saccharomyces cerevisiae, however, it is unclear how prions affect genome-wide transcription. We show here that the prion ([SWI+]) and mutant (swi1∆) forms of Swi1, a subunit of the SWI/SNF chromatin-remodeling complex, confer dramatically distinct transcriptomic profiles. In [SWI+] cells, genes encoding for 34 transcription factors (TFs) and 24 Swi1-interacting proteins can undergo transcriptional modifications. Several TFs show enhanced aggregation in [SWI+] cells. Further analyses suggest that such alterations are key factors in specifying the transcriptomic signatures of [SWI+] cells. Interestingly, swi1∆ and [SWI+] impose distinct and oftentimes opposite effects on cellular functions. Translation-associated activities, in particular, are significantly reduced in swi1∆ cells. Although both swi1∆ and [SWI+] cells are similarly sensitive to thermal, osmotic and drought stresses, harmful, neutral or beneficial effects were observed for a panel of tested chemical stressors. Further analyses suggest that the environmental stress response (ESR) is mechanistically different between swi1∆ and [SWI+] cells—stress-inducible ESR (iESR) are repressed by [SWI+] but unchanged by swi1∆ while stress-repressible ESR (rESR) are induced by [SWI+] but repressed by swi1∆. Our work thus demonstrates primarily gain-of-function outcomes through transcriptomic modifications by [SWI+] and highlights a prion-mediated regulation of transcription and phenotypes in yeast.
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影响因子:
64.5
作者:
Cai X;Chen J;Xu H;Liu S;Jiang QX;Halfmann R;Chen ZJ
通讯作者:
Chen ZJ
DOI:
10.1093/bioinformatics/btu638
发表时间:
2015-01-15
期刊:
Bioinformatics (Oxford, England)
影响因子:
--
作者:
Anders S;Pyl PT;Huber W
通讯作者:
Huber W
影响因子:
30.8
作者:
Du, Zhiqiang;Park, Kyung-Won;Li, Liming
通讯作者:
Li, Liming
影响因子:
8.6
作者:
Du, Zhiqiang;Valtierra, Stephanie;Li, Liming
通讯作者:
Li, Liming
影响因子:
3.3
作者:
Du, Zhiqiang;Li, Liming
通讯作者:
Li, Liming