ArticleBiology of reproduction2013
Loss of R2D2 proteins ROPN1 and ROPN1L causes defects in murine sperm motility, phosphorylation, and fibrous sheath integrity.
Article in Biology of reproduction, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers.
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Who cites it
56 citing papers in PubMed, 105 citations in OpenAlex.
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- Structure and Composition of Spermatozoa Fibrous Sheath in Diverse Groups of Metazoa.International journal of molecular sciences · 2024Review
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- Sperm long non-coding RNAs as markers for ram fertility.Frontiers in veterinary science · 2024Article
- CCDC146 is required for sperm flagellum biogenesis and male fertility in mice.Cellular and molecular life sciences : CMLS · 2023Article
- WNK1 is required during male pachynema to sustain fertility.iScience · 2023Article
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- Deficiency of cancer/testis antigen gene CT55 causes male infertility in humans and mice.Cell death and differentiation · 2023Article
- Comparative proteomic analysis of seminal plasma exosomes in buffalo with high and low sperm motility.BMC genomics · 2023Article
- RNA sequencing profiles reveals progressively reduced spermatogenesis with progression in adult cryptorchidism.Frontiers in endocrinology · 2023Article
- IRGC1, a testis-enriched immunity related GTPase, is important for fibrous sheath integrity and sperm motility in mice.Developmental biology · 2022Article
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
The fibrous sheath (FS) is a flagellar cytoskeletal structure unique to sperm that surrounds the outer dense fibers and axoneme. Its primary components are A-kinase anchoring proteins (AKAPs) 3 and 4, which suggests that the FS affects flagellar beating via the scaffolding of signaling pathways necessary for motility. Sperm proteins ROPN1 and ROPN1L bind AKAP3. To determine the role of ROPN1 and ROPN1L in sperm function, we created mice deficient in ROPN1 (RKO), mice deficient in ROPN1L (RLKO), and double knockout mice (DKO). All three strains of mice had normal testicular morphology and spermatogenesis. Only the DKOs had obvious defects in sperm morphology (thinning and shredding of the principal piece), which was accompanied by a reduction in AKAP3 levels. RLKO mice had slightly reduced sperm motility and increased levels of ROPN1. RKO mice had moderately impaired motility and increased levels of ROPN1L. DKO sperm were immotile. We have previously determined that RKO male mice are subfertile, and DKO males are infertile. Together these data indicate that ROPN1L and ROPN1 compensate for each other in the absence of the opposing protein, possibly to maintain AKAP3 incorporation in the FS. Sperm from mice lacking ROPN1L exhibited reductions in both cAMP-dependent protein kinase (PKA) phosphorylation of a 270-kDa protein (perhaps FSCB), and in capacitation-induced tyrosine phosphorylation. Sperm from mice lacking ROPN1 had reduced levels of FSCB and increased tyrosine phosphorylation of noncapacitated sperm. These data demonstrate that mutations in ROPN1 and ROPN1L can cause defects in FS integrity, sperm motility, and PKA-dependent signaling processes, leading to male infertility.
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