TFEB将自与溶酶体生物发生联系起来
Carmine Settembre1, Chiara Di Malta, Vinicia Assunta Polito
1Telethon Institute of Genetics and Medicine (TIGEM), Via Pietro Castellino 111, 80131 Naples, Italy.
Science (New York, N.Y.)
|May 28, 2011
概括
饥饿会触发一种称为自的细胞过程,通过协调自和溶酶体来增强降解. 这由转录因子EB (TFEB) 和一种对营养素敏感的激酶通路控制.
科学领域:
- 细胞生物学 细胞生物学
- 分子生物学分子生物学
- 生物化学 生物化学
背景情况:
- 自是一种基本的细胞代谢过程,涉及自和溶酶体.
- 细胞饥饿通过扩大这些细胞器来增强退化.
- 正在研究调节这种协调反应的精确分子机制.
研究的目的:
- 阐明控制自的被饥饿激活的转录程序.
- 为了确定关键的调节器协调自和溶酶体功能在饥饿期间.
- 调查控制这一关键调节器活动的信号通路.
主要方法:
- 转录分析,以识别饥饿诱导的基因.
- 溶酶体和自基因表达的分析.
- 西方涂抹和免疫光检测以评估蛋白质局部化和酸化.
- 药物抑制和信号通路的基因操纵.
主要成果:
- 饥饿激活了一种转录程序,该程序控制着自细胞形成, lysosome-autophagosome融合和基质降解.
- 转录因子EB (TFEB) 是溶酶体生物发生的主调节者,它协调了这个程序.
- 细胞外信号调节激酶2 (ERK2) 酸化TFEB,调节其核定位和活性.
- ERK2活动由细胞外营养水平调节,将营养感应与自联系起来.
结论:
- 一个依赖于线粒激活蛋白激酶 (MAPK) 的途径调节了自.
- 这一途径控制了溶酶体和自酶体的生物发生以及它们的功能伙伴关系.
- TFEB充当中央协调员,根据营养的可用性,整合 lysosomal 和自的途径.
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