ArticleFrontiers in cell and developmental biology2023
Knock-down of YME1L1 induces mitochondrial dysfunction during early porcine embryonic development.
Article in Frontiers in cell and developmental biology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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4 citing papers in PubMed, 2 citations in OpenAlex.
- YME1L1 degradation by TRIM21 inhibits bladder cancer proliferation, metastasis, and mitochondrial function.Oncogene · 2026Article
- Proteolytic control of mitochondrial protein translocases.Protein science : a publication of the Protein Society · 2026Review
- Integrative Transcriptomic Analysis Identifies Novel Mitochondrial Gene Targets in Parkinson's Disease.Molecular neurobiology · 2026Article
- Targeted Sirtuin 3 Activation by Biomimetic Black Phosphorus Nanosheets Mitigates Sepsis-Induced Acute Kidney Injury through Yeast Mitochondrial Escape 1-Like 1 Deacetylation.Biomaterials research · 2026Article
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Authors and funding
9 authors at 1 institution in 1 country.
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Abstract
YME1L1, a mitochondrial metalloproteinase, is an Adenosine triphosphate (ATP)-dependent metalloproteinase and locates in the mitochondrial inner membrane. The protease domain of YME1L1 is oriented towards the mitochondrial intermembrane space, which modulates the mitochondrial GTPase optic atrophy type 1 (OPA1) processing. However, during embryonic development, there is no report yet about the role of YME1L1 on mitochondrial biogenesis and function in pigs. In the current study, the mRNA level of YME1L1 was knocked down by double strand RNA microinjection to the 1-cell stage embryos. The expression patterns of YME1L1 and its related proteins were performed by immunofluorescence and western blotting. To access the biological function of YME1L1, we first counted the preimplantation development rate, diameter, and total cell number of blastocyst on day-7. First, the localization of endogenous YME1L1 was found in the punctate structures of the mitochondria, and the expression level of YME1L1 is highly expressed from the 4-cell stage. Following significant knock-down of YME1L1, blastocyst rate and quality were decreased, and mitochondrial fragmentation was induced. YME1L1 knockdown induced excessive ROS production, lower mitochondrial membrane potential, and lower ATP levels. The OPA1 cleavage induced by YME1L1 knockdown was prevented by double knock-down of YME1L1 and OMA1. Moreover, cytochrome
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