ArticleDevelopmental biology2024
ARF6, a component of intercellular bridges, is essential for spermatogenesis in mice.
Article in Developmental biology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
3 citing papers in PubMed, 6 citations in OpenAlex.
- The formation and function of intercellular bridges in male germlines.Communications biology · 2026Review
- Microfilament-Myosin II Regulates the Differentiation of Multinucleated Cysts into Oocytes and Influences Oocyte Developmental Potential in Mice.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- A key role for centralspindlin and Ect2 in the development of multicellularity and the emergence of Metazoa.Current biology : CB · 2025Article
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Male germ cells are connected by intercellular bridges (ICBs) in a syncytium due to incomplete cytokinesis. Syncytium is thought to be important for synchronized germ cell development by interchange of cytoplasmic factors via ICBs. Mammalian ADP-ribosylation factor 6 (ARF6) is a small GTPase that is involved in many cellular mechanisms including but not limited to regulating cellular structure, motility, vesicle trafficking and cytokinesis. ARF6 localizes to ICBs in spermatogonia and spermatocytes in mice. Here we report that mice with global depletion of ARF6 in adulthood using Ubc-CreERT2 display no observable phenotypes but are male sterile. ARF6-deficient males display a progressive loss of germ cells, including LIN28A-expressing spermatogonia, and ultimately develop Sertoli-cell-only syndrome. Specifically, intercellular bridges are lost in ARF6-deficient testis. Furthermore, germ cell-specific inactivation using the Ddx4-CreERT2 results in the same testicular morphological phenotype, showing the germ cell-intrinsic requirement of ARF6. Therefore, ARF6 is essential for spermatogenesis in mice and this function is conserved from Drosophila to mammals.
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