fzo-1/Mfn2是负责线粒体外膜融合的蛋白，其突变会直接导致线粒体持续片段化及膜电势的急剧降低，进而影响ATP合成及细胞正常生理功能。

2024年7月2日 · 在这项工作中，我们通过普遍过表达线粒体裂变基因 drp-1 或线粒体融合基因 fzo-1 和 eat-3 单独或组合来研究增加线粒体裂变或线粒体融合能力的影响。 然后我们测量了线粒体功能、线粒体网络形态、生理速率、抗逆性和寿命。

2019年6月19日 · Specialized dynamin GTPases FZO-1/Mitofusin and EAT-3/OPA-1 mediate fusion, while DRP-1 is required for fission .

2021年6月21日 · To test whether disruption of mitochondrial dynamics in subtypes of neurons is sufficient to induce nonautonomous UPR mt, we triggered fzo-1 RNAi using the unc-17, eat-4, tph-1, or tdc-1 promoter; fzo-1 RNAi specifically in the cholinergic, serotonergic, or glutamatergic neurons, but not the tyraminergic neurons, induced nonautonomous UPR mt ...

2017年8月31日 · Thus, we assessed the fermentative (glucose) and respiratory (glycerol) growth capacities of three distinct N-terminal deletion mutant strains of FZO1, namely fzo1Δ 1–30, fzo1Δ 1–60 and ...

2004年12月10日 · Mutations of the fzo gene in flies inhibit mitochondrial fusion during spermatogenesis, leading to a “fuzzy onion” morphology (18). A homolog of Fzo1 protein is found in mammals (e.g. rat Fzo1 and human Mfn) (19, 20).

2023年3月27日 · upr是由转录因子atfs-1(与应激-1相关的激活转录因子)介导的，它包含线粒体定位序列(mts)和核定位序列(nls) 。 在没有线粒体应激的情况下，ATFS-1被导入线粒体，在那里被线粒体Lon蛋白酶降解。

2021年6月21日 · Here, we show that in C. elegans, loss of neuronal fzo-1/mitofusin induces nonautonomous UPR mt through multiple neurotransmitters and neurohormones, including acetylcholine, serotonin, glutamate, tyramine, and insulin-like peptides. Neuronal fzo-1 depletion also triggers nonautonomous mitochondrial fragmentation, which requires autophagy and ...

2004年12月10日 · Mitochondrial morphology and physiology are regulated by the processes of fusion and fission. Some forms of apoptosis are reported to be associated with mitochondrial fragmentation. We showed that overexpression of Fzo1A/B (rat) proteins involved in mitochondrial fusion, or silencing of Dnm1 (rat)/D …

2020年2月26日 · The fragmented mitochondria and accelerated wound closure of fzo-1 mutants are dependent on MIRO-1 function. Genetic and transcriptomic analyzes show that enhanced mitochondrial fragmentation accelerates wound closure via the upregulation of mtROS and Cytochrome P450.