题目内容

真核生物催化tRNA转录的酶是:

A. DNA聚合酶
B. RNA 聚合酶I
C. RNA聚合酶Ⅲ
D. RNA聚合酶Ⅱ
E. DNA聚合酶I

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更多问题

启动子是指:

A. DNA复制开始的序列
B. RNA转录起始的序列
C. 蛋白质翻译起始的序列
DNA模板结合RNA聚合酶的序列
E. DNA模板结合DNA聚合酶的序列

对鹅膏蕈碱最敏感的酶是:

A. RNA聚合酶Ⅱ
B. RNA聚合酶I
C. RNA聚合酶Ⅲ
DNA聚合酶I
E. DNA聚合酶Ⅱ

参与转录的物质有

A. NTP
B. NMP
C. 单链DNA模板
DNA指导的RNA聚合酶

In eukaryotes, autophagy maintains cellular homeostasis by recycling cytoplasmic components. The autophagy-related proteins (ATGs) ATG1 and ATG13 form a protein kinase complex that regulates autophagosome formation; however, mechanisms regulating ATG1 and ATG13 remain poorly understood. Here, we show that, under different nutrient conditions, the RING-type E3 ligases SEVEN IN ABSENTIA OF ARABIDOPSIS THALIANA1 (SINAT1), SINAT2, and SINAT6 control ATG1 and ATG13 stability and autophagy dynamics by modulating ATG13 ubiquitylation in Arabidopsis (Arabidopsis thaliana). During prolonged starvation and recovery, ATG1 and ATG13 were degraded through the 26S proteasome pathway. TUMOR NECROSIS FACTOR RECEPTOR ASSOCIATED FACTOR1a (TRAF1a) and TRAF1b interacted in planta with ATG13a and ATG13b and required SINAT1 and SINAT2 to ubiquitylate and degrade ATG13s in vivo. Moreover, lysines K607 and K609 of ATG13a protein contributed to K48-linked ubiquitylation and destabilization, and suppression of autophagy. Under starvation conditions, SINAT6 competitively interacted with ATG13 and induced autophagosome biogenesis. Furthermore, under starvation conditions, ATG1 promoted TRAF1a protein stability in vivo, suggesting feedback regulation of autophagy. Consistent with ATGs functioning in autophagy, theatg1a atg1b atg1ctriple knockout mutants exhibited premature leaf senescence, hypersensitivity to nutrient starvation, and reduction in TRAF1a stability. Therefore, these findings demonstrate that SINAT family proteins facilitate ATG13 ubiquitylation and stability and thus regulate autophagy.

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