ArticlePLoS genetics2010
Sex reversal in zebrafish fancl mutants is caused by Tp53-mediated germ cell apoptosis.
Article in PLoS genetics, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 103 papers, 1 of them a synthesis that pooled it.
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Who cites it
103 citing papers in PubMed, 1 synthesis or guideline pooled it, 230 citations in OpenAlex.
- Sex-specific differences in zebrafish brains.Biology of sex differences · 2022Pooled it
- MEIOSIN retains a STRA8-independent activity that contributes to meiotic gene activation across vertebrates.Genes & development · 2026Article
- Full-Length Transcriptome Comparison of Male and Female Gonads inBiomolecules · 2026Article
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- Stn1 promotes zebrafish oocyte development via amplifying Wnt/β-catenin signaling.EMBO reports · 2026Article
- An mTOR-Stat3-Stathmin pathway controls centrosome and microtubule dynamics for oocyte polarization.Current biology : CB · 2025Article
- Tatdn2 is required for DNA repair to safeguard genome stability in primordial germ cells.Nucleic acids research · 2025Article
- Zebrafish Unga Is Required for Genomic Maintenance upon Genotoxic Stress and Male Fertility.Journal of developmental biology · 2025Article
- Distinct cellular and reproductive consequences of meiotic chromosome synapsis defects in syce2 and sycp1 mutant zebrafish.PLoS genetics · 2025Article
- Regulation of early gonocyte differentiation in zebrafish.Biochemical Society transactions · 2025Article
- Meioc-Piwil1 complexes regulate rRNA transcription for differentiation of spermatogonial stem cells.eLife · 2025Article
- Single-cell transcriptomes of zebrafish germline reveal progenitor types and feminization by Foxl2l.eLife · 2025Article
- Clonal analysis reveals differential PGC contributions to the early germline and ovarian reserve.bioRxiv : the preprint server for biology · 2025Article
- Zglp-1 is a novel essential transcriptional regulator for sex reversal in zebrafish.Marine life science & technology · 2025Article
- Exploring the Fanconi Anemia Gene Expression and Regulation by MicroRNAs in Gilthead Seabream (Sparus aurata) at Different Gonadal Development Stages.Marine biotechnology (New York, N.Y.) · 2025Article
- Variant ribosomal DNA is essential for female differentiation in zebrafish.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2025Article
- The piRNA protein Asz1 is essential for germ cell and gonad development in zebrafish and exhibits differential necessities in distinct types of germ granules.PLoS genetics · 2025Article
- Cellular retinoic acid-binding proteins regulate germ cell proliferation and sex determination in zebrafish.Development (Cambridge, England) · 2024Article
- Adamts9 is required for the development of primary ovarian follicles and maintenance of female sex in zebrafish†.Biology of reproduction · 2024Article
- Developmental Delay and Male-Biased Sex Ratio inGenes · 2024Article
43 more citing papers are in PubMed but not listed here.
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Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
Abstract
The molecular genetic mechanisms of sex determination are not known for most vertebrates, including zebrafish. We identified a mutation in the zebrafish fancl gene that causes homozygous mutants to develop as fertile males due to female-to-male sex reversal. Fancl is a member of the Fanconi Anemia/BRCA DNA repair pathway. Experiments showed that zebrafish fancl was expressed in developing germ cells in bipotential gonads at the critical time of sexual fate determination. Caspase-3 immunoassays revealed increased germ cell apoptosis in fancl mutants that compromised oocyte survival. In the absence of oocytes surviving through meiosis, somatic cells of mutant gonads did not maintain expression of the ovary gene cyp19a1a and did not down-regulate expression of the early testis gene amh; consequently, gonads masculinized and became testes. Remarkably, results showed that the introduction of a tp53 (p53) mutation into fancl mutants rescued the sex-reversal phenotype by reducing germ cell apoptosis and, thus, allowed fancl mutants to become fertile females. Our results show that Fancl function is not essential for spermatogonia and oogonia to become sperm or mature oocytes, but instead suggest that Fancl function is involved in the survival of developing oocytes through meiosis. This work reveals that Tp53-mediated germ cell apoptosis induces sex reversal after the mutation of a DNA-repair pathway gene by compromising the survival of oocytes and suggests the existence of an oocyte-derived signal that biases gonad fate towards the female developmental pathway and thereby controls zebrafish sex determination.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.