ArticleNature cell biology2023
Mitopherogenesis, a form of mitochondria-specific ectocytosis, regulates sperm mitochondrial quantity and fertility.
Article in Nature cell biology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.
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Who cites it
37 citing papers in PubMed, 53 citations in OpenAlex.
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- A RAF-SnRK2-PP2C functional module regulates cell survival in the chlorophyte Chlamydomonas reinhardtii.The New phytologist · 2026Article
- TFEB Deficiency Impairs Male Fertility Through Mitochondrial Dysfunction.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026Article
- DDI-4 induces a temperature-sensitive exocytotic remodeling during C. elegans spermiogenesis via nsun-2-dependent sphingosine signaling.PLoS genetics · 2026Article
- The intrinsically disordered protein SPE-56 is required for acrosomal-like exocytosis and fertility in Caenorhabditis elegans.Scientific reports · 2026Article
- Rethinking Mitochondria: The Extracellular Dimension.Circulation research · 2026Review
- Mitochondria-Derived Vesicles and Mitochondrial Extracellular Vesicles in Health and Cardiovascular Disease.Circulation research · 2026Review
- Extracellular vesicles in cancer progression: mechanisms and significance.Science China. Life sciences · 2026Review
- An extracellular vesicle-mediated mitochondrial transfer network critical for testosterone synthesis.Nature cell biology · 2026Article
- Vesicles for cell crosstalk in bone: composition, function and application.Science China. Life sciences · 2026Review
- The mechanisms and functions of mitochondria-encapsulating extracellular vesicles.Science China. Life sciences · 2026Review
- A decade of discovery: tracing the footmarks of migrasomes, unveiling the footprints of cells.Science China. Life sciences · 2026Review
- ATG5-HSP90.2-mediated micromitophagy as a cytological basis for maternal inheritance of plant mitochondria.Nature plants · 2026Article
- Mitochondria beyond boundaries: from cellular powerhouses to intercellular messengers in health and disease.Science China. Life sciences · 2026Review
- ALKB-1-dependent tRNA methylation is required for efficient paternal mitochondrial elimination.Nature communications · 2026Article
- Mitochondrial components secretion in extracellular vesicles promotes alveolar epithelial mitochondrial quality control.Nature communications · 2025Article
- Clinical relevance of extracellular vesicles in cancer - therapeutic and diagnostic potential.Nature reviews. Clinical oncology · 2025Review
- Upregulation of miR-151a-5p in high DFI sperm induces DNA damage and mitochondrial dysfunction by targeting INPP4B and VAMP1.Reproductive biology and endocrinology : RB&E · 2025Article
- Progress of research on engineered extracellular vesicles from different sources for disease treatment.Histology and histopathology · 2025Review
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Authors and funding
12 authors at 2 institutions in 1 country.
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Abstract
Mitochondrial export into the extracellular space is emerging as a fundamental cellular process implicated in diverse physiological activities. Although a few studies have shed light on the process of discarding damaged mitochondria, how mitochondria are exported and the functions of mitochondrial release remain largely unclear. Here we describe mitopherogenesis, a formerly unknown process that specifically secretes mitochondria through a unique extracellular vesicle termed a 'mitopher'. We observed that during sperm development in male Caenorhabditis elegans, healthy mitochondria are exported out of the spermatids through mitopherogenesis and each of the generated mitophers harbours only one mitochondrion. In mitopherogenesis, the plasma membrane first forms mitochondrion-embedding outward buds, which then promptly bud off and thereby result in the generation of mitophers. Mechanistically, extracellular protease signalling in the testis triggers mitopher formation from spermatids, which is partially mediated by the tyrosine kinase SPE-8. Moreover, mitopherogenesis requires normal microfilament dynamics, whereas myosin VI antagonizes mitopher generation. Strikingly, our three-dimensional electron microscopy analyses indicate that mitochondrial quantity requires precise modulation during sperm development, which is critically mediated by mitopherogenesis. Inhibition of mitopherogenesis causes accumulation of mitochondria in sperm, which may lead to sperm motility and fertility defects. Our findings identify mitopherogenesis as a previously undescribed process for mitochondria-specific ectocytosis, which may represent a fundamental branch of mechanisms underlying mitochondrial quantity control to regulate cell functions during development.
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