ArticleGenome biology2024
N6-methyladenosine writer METTL16-mediated alternative splicing and translation control are essential for murine spermatogenesis.
Article in Genome biology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed.
- O-GlcNAc transferase governs spermatogenic mitotic-to-meiotic transition and progression by coordinating transcription and alternative splicing programs.Cellular & molecular biology letters · 2026Article
- mJournal of assisted reproduction and genetics · 2026Review
- Methamphetamine-induced inhibition of Mettl21c in undifferentiated spermatogonia impairs male fertility in mice.Asian journal of andrology · 2026Article
- The role of m6A modification in spermatogenic dysfunction.Molecular biology reports · 2026Review
- Quercetin upregulates steroid hormone biosynthesis to enhance reproductive performance in roosters.Poultry science · 2026Article
- Article
- METTL16 in cancer: Roles and regulatory mechanisms.Genes & diseases · 2026Review
- Genome-wide identification and expression analysis of YTH gene family in barley reveals their potential role under abiotic stresses.Genetica · 2026Article
- PCID2 is essential for spermatogonial differentiation by regulating alternative splicing.Cellular and molecular life sciences : CMLS · 2026Article
- The intricate dance of RNA-binding proteins: unveiling the mechanisms behind male infertility.Human reproduction update · 2026Review
- Transcriptome-Wide Identification and Analysis Reveals mVeterinary sciences · 2025Article
- Research progress on m6A RNA methylation modification in human reproduction related diseases.European journal of medical research · 2025Review
- Targeting METTL16 attenuates mesangial cell viability and fibrosis in a high-glucose state by suppressing m6A modification and the expression of RAP1B.BMC molecular and cell biology · 2025Article
- mAdvanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Metabolomic Analysis of Cauda Epididymal Fluid in Yaks and Cattle.Animals : an open access journal from MDPI · 2025Article
- PPP6R3-mediated dephosphorylation regulates mRNA translation during spermatogonial differentiation.Communications biology · 2025Article
- Comparative Analysis of Testicular Transcriptional and Translational Landscapes in Yak and Cattle-Yak: Implications for Hybrid Male Sterility.Biomolecules · 2025Article
- METTL16 and YTHDC1 Regulate Spermatogonial Differentiation via m6A.Cell proliferation · 2025Article
- METTL16 is Required for Meiotic Sex Chromosome Inactivation and DSB Formation and Recombination during Male Meiosis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- The Intricate Functional Networks of Pre-mRNA Alternative Splicing in Mammalian Spermatogenesis.International journal of molecular sciences · 2024Review
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15 authors.
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Abstract
backgroundThe mitosis-to-meiosis switch during spermatogenesis requires dynamic changes in gene expression. However, the regulation of meiotic transcriptional and post-transcriptional machinery during this transition remains elusive.
resultsWe report that methyltransferase-like protein 16 (METTL16), an N6-methyladenosine (m6A) writer, is required for mitosis-to-meiosis transition during spermatogenesis. Germline conditional knockout of Mettl16 in male mice impairs spermatogonial differentiation and meiosis initiation. Mechanistically, METTL16 interacts with splicing factors to regulate the alternative splicing of meiosis-related genes such as Stag3. Ribosome profiling reveals that the translation efficiency of many meiotic genes is dysregulated in METTL16-deficient testes. m6A-sequencing shows that ablation of METTL16 causes upregulation of the m6A-enriched transcripts and downregulation of the m6A-depleted transcripts, similar to Meioc and/or Ythdc2 mutants. Further in vivo and in vitro experiments demonstrate that the methyltransferase activity site (PP185-186AA) of METTL16 is necessary for spermatogenesis.
conclusionsOur findings support a molecular model wherein the m6A writer METTL16-mediated alternative splicing and translation efficiency regulation are required to control the mitosis-to-meiosis germ cell fate decision in mice, with implications for understanding meiosis-related male fertility disorders.
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