C. elegans as a model to study mitochondrial biology and disease

被引:13
|
作者
Onraet, Tessa [1 ]
Zuryn, Steven [1 ]
机构
[1] Univ Queensland, Queensland Brain Inst, Clem Jones Ctr Ageing Dementia Res, Brisbane 4072, Australia
基金
澳大利亚国家健康与医学研究理事会;
关键词
Mitochondrial disease; Neurodegeneration; Proteotoxicity; Aging; Fission; Fusion; UPRmt; MtDNA; Biogenesis; Mitophagy; CAENORHABDITIS-ELEGANS; PATERNAL MITOCHONDRIA; LIFE-SPAN; INNATE IMMUNITY; MITOPHAGY; PROTEIN; AUTOPHAGY; HETEROPLASMY; DEGRADATION; MAINTENANCE;
D O I
10.1016/j.semcdb.2023.04.006
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
Mitochondria perform a myriad of essential functions that ensure organismal homeostasis, including maintaining bioenergetic capacity, sensing and signalling the presence of pathogenic threats, and determining cell fate. Their function is highly dependent on mitochondrial quality control and the appropriate regulation of mitochondrial size, shape, and distribution during an entire lifetime, as well as their inheritance across generations. The roundworm Caenorhabditis elegans has emerged as an ideal model organism through which to study mitochon-dria. The remarkable conservation of mitochondrial biology has allowed C. elegans researchers to investigate complex processes that are challenging to study in higher organisms. In this review, we explore the key recent contributions of C. elegans to mitochondrial biology through the lens of mitochondrial dynamics, organellar removal, and mitochondrial inheritance, as well as their involvement in immune responses, various types of stress, and transgenerational signalling.
引用
收藏
页码:48 / 58
页数:11
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