生物
线粒体DNA
突变体
线粒体
基因
表型
细胞生物学
基因表达
遗传学
突变
作者
Khandaker Ashfaqul Muid,Önder Kimyon,Shahadat Hasan Reza,Hüseyin Çağlar Karakaya,Ahmet Koç
出处
期刊:Gene
[Elsevier]
日期:2019-07-01
卷期号:706: 172-180
被引量:8
标识
DOI:10.1016/j.gene.2019.05.001
摘要
Molecular mechanisms of aging and longevity are still mostly unknown. Mitochondria play central roles in cellular metabolism and aging. In this study, we identified three deletion mutants of mitochondrial metabolism genes (ppa2∆, dss1∆, and afg3∆) that live longer than wild-type cells. These long-lived cells harbored significantly decreased amount of mitochondrial DNA (mtDNA) and reactive oxygen species (ROS). Compared to the serpentine nature of wild-type mitochondria, a different dynamics and distribution pattern of mitochondria were observed in the mutants. Both young and old long-lived cells produced relatively low but adequate levels of ATP for cellular activities. The status of the retrograde signaling was checked by expression of CIT2 gene and found activated in long-lived mutants. The mutant cells were also profiled for their gene expression patterns, and genes that were differentially regulated were determined. All long-lived cells comprised similar pleiotropic phenotype regarding mitochondrial dynamics and functions. Thus, this study suggests that DSS1, PPA2, and AFG3 genes modulate the lifespan by altering the mitochondrial morphology and functions.
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