The yeast chromatin remodeler Rsc1-RSC complex is required for transcriptional activation of autophagy-related genes and inhibition of the TORC1 pathway in response to nitrogen starvation.
The yeast chromatin remodeler Rsc1-RSC complex is required for transcriptional activation of autophagy-related genes and inhibition of the TORC1 pathway in response to nitrogen starvation.
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DOI：
10.1016/j.bbrc.2015.07.114
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发表时间：
2015-09
影响因子：
3.1
通讯作者：
F. Yu;Yuko Imamura;M. Ueno;Sho W. Suzuki;Y. Ohsumi;M. Yukawa;E. Tsuchiya
中科院分区：
文献类型：
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作者：
F. Yu;Yuko Imamura;M. Ueno;Sho W. Suzuki;Y. Ohsumi;M. Yukawa;E. Tsuchiya
酵母RSC是一种依赖atp的染色质重塑复合体，对有丝分裂和减数分裂的生长至关重要。该复合体有两种不同的同工异构体，由Rsc1或Rsc2的存在决定；然而，这些复合物之间的功能差异尚不清楚。我们发现含有Rsc1而不含Rsc2的RSC复合物在自噬诱导中起作用。Rsc1不仅是atg8mrna完全表达所必需的，也是维持Atg8蛋白稳定性所必需的。有趣的是，自噬活性的降低和Atg8蛋白稳定性inrsc1Δcells，而不是atg8mrna表达的缺陷，被tor1的缺失部分抑制。此外，我们发现thatrsc1Δimpaired Rho GTPase Rho1与TORC1特异性组分Kog1之间的结合，这是下调TORC1活性所必需的。这些结果表明，含有rsc1的RSC复合物在适当诱导自噬中发挥双重作用：1)独立于TORC1途径的自噬相关基因的转录激活，2)TORC1的失活，可能通过增强Rho1-Kog1结合。
The yeast RSC, an ATP-dependent chromatin-remodeling complex, is essential for mitotic and meiotic growth. There are two distinct isoforms of this complex defined by the presence of either Rsc1 or Rsc2; however, the functional differences between these complexes are unclear. Here we show that the RSC complex containing Rsc1, but not Rsc2, functions in autophagy induction. Rsc1 was required not only for full expression ofATG8mRNA but also for maintenance of Atg8 protein stability. Interestingly, decreased autophagic activity and Atg8 protein stability inrsc1Δcells, but not the defect inATG8mRNA expression, were partially suppressed by deletion ofTOR1. In addition, we found thatrsc1Δimpaired the binding between the Rho GTPase Rho1 and the TORC1-specific component Kog1, which is required for down-regulation of TORC1 activity. These results suggest that the Rsc1-containing RSC complex plays dual roles in the proper induction of autophagy: 1) the transcriptional activation of autophagy-related genes independent of the TORC1 pathway and 2) the inactivation of TORC1, possibly through enhancement of Rho1-Kog1 binding.