The autophagy gene product BEC-1 supports normal aging and neurodevelopment in Caenorhabditis elegans II
The autophagy gene product BEC-1 supports normal aging and neurodevelopment in Caenorhabditis elegans II
复制标题
自噬基因产物 BEC-1 支持秀丽隐杆线虫 II 的正常衰老和神经发育
作者：
Nicholas A. Ashley;A. Holgado
描述巨自噬（Macroautophagy）（以下简称自噬）是一种细胞管家机制，其使用双膜靶向并吞噬细胞产物以形成自噬体。然后，这些双膜细胞器与溶酶体融合，在那里细胞产物被降解和回收（中村和Yoshimori，2018）。运动皮质中自噬功能的丧失与帕金森病神经退行性症状的进展相关（Kaila and Lang 2015; Fahn et al. 2004）。为了更好地理解Beclin 1和自噬在神经元中的作用，我们研究了C。BEC-1的线虫突变体。纯合（bec-1 -/-）和杂合bec-1（ok 691）（bec-1 +/-）突变体的运动均显示出显著缺陷（图1）。纯合子bec-1（ok 691）突变体在成年后1-7天的向后运动速率范围为3-8次身体弯曲/分钟，杂合子bec-1（ok 691）突变体在相当年龄为6-9次身体弯曲/分钟。这些运动缺陷表明自噬控制神经元依赖性行为的作用。
Description Macroautophagy (hereon referred as Autophagy) is a cellular housekeeping mechanism that uses a double membrane to target and engulf cell products for the formation of autophagosomes. These double membrane organelles then fuse to lysosomes where cell products are degraded and recycled (Nakamura and Yoshimori, 2018). The loss of autophagy function in the motor cortex has been associated with progression of neurodegenerative symptoms in Parkinson’s disease (Kaila and Lang 2015; Fahn et al. 2004). To better understand the role of Beclin 1 and autophagy in neurons, we studied locomotion in C. elegans mutants for bec-1. Locomotion in both homozygous (bec-1 -/-) and heterozygous bec-1(ok691) (bec-1 +/-) mutants showed significant defects (Figure 1). Homozygous bec-1(ok691) mutants backwards locomotion rates ranged between 3-8 body bends/minute at ages 1-7 days of adulthood and heterozygous bec-1(ok691) mutants were 6-9 body bends/minute at comparable ages. These defects in locomotion suggest a role of autophagy controlling behaviors that are neuronal dependent.
DOI：
10.1056/nejmoa033447
发表时间：
2004-12
期刊：
The New England journal of medicine
影响因子：
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作者：
S. Fahn;D. Oakes;I. Shoulson;K. Kieburtz;A. Rudolph;A. Lang;C. Olanow;C. Tanner;K. Marek
通讯作者：
S. Fahn;D. Oakes;I. Shoulson;K. Kieburtz;A. Rudolph;A. Lang;C. Olanow;C. Tanner;K. Marek