ID OF RIBOSOMAL TRANSLATION INITIATION FACTORS BY TANDEM MASS SPECTROMETRY

通过串联质谱鉴定核糖体翻译起始因子

• 批准号: 6348286
• 负责人: JOHN R YATES
• 金额: $ 0.33万
• 依托单位: UNIVERSITY OF WASHINGTON
• 依托单位国家: 美国
• 财政年份: 2000
• 资助国家: 美国
• 起止时间: 2000-09-01 至 2001-08-31
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/6348286
• 关键词: bioengineering /biomedical engineering; biomedical resource; enzymes; plants; proteins

Mitochondrial inheritance is a the process whereby mitochondria, self-replicating organelles essential for growth, move from mother to daughter cells during cell division. We determined the Arp2/3 complex, an evolutionarily conserved complex implicated in actin dependent movement is a component of the mitochondrial motility machinery. The Arc15 subunit of the Arp2/3/ complex was recovered from salt extracted mitochondrial peripheral membrane proteins by F-actin chromatography. Arc15 is not essential for viability or actin cytoskeletal organization. However, deletion of Arc15 causes loss of growth on non-fermentable carbon sources, loss of all directed mitochondrial movement, and defects in mitochondrial morphology and motility. In addition, Arp co-localizes with mitochondria. Our studies support a novel mechanism for actin-based organelle motility: Arp2/3 complex control of mitochondrial movement and inheritance.

线粒体遗传是一个线粒体， 自我复制的细胞器对生长至关重要，从母亲转移到 细胞分裂期间的子细胞。 我们确定了Arp 2/3 复合物，一种进化上保守的与肌动蛋白有关的复合物 依赖性运动是线粒体运动的一个组成部分 机械. 回收Arp 2/3/复合物的Arc 15亚基 从盐提取的线粒体外周膜蛋白， F-肌动蛋白层析。 ARC 15对细胞活力或肌动蛋白 细胞骨架组织 然而，删除Arc 15会导致 非发酵性碳源的增长，所有定向碳源的损失 线粒体运动和线粒体形态缺陷， 能动性 此外，阿普与线粒体共定位。 我们 研究支持一种基于肌动蛋白的细胞器运动的新机制： Arp 2/3复合体控制线粒体运动和遗传。