ArticleNature communications2016
ALDH1A1 provides a source of meiosis-inducing retinoic acid in mouse fetal ovaries.
Article in Nature communications, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.
What it found
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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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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
43 citing papers in PubMed, 94 citations in OpenAlex.
- Circular RNA-Mediated ceRNA networks predict sperm retrieval outcomes in non-obstructive azoospermia.Journal of assisted reproduction and genetics · 2026Article
- Molecular genetics of meiotic initiation in mammals.Biology of reproduction · 2026Article
- MEIOC prevents continued mitotic cycling and promotes meiotic entry during mouse oogenesis.Development (Cambridge, England) · 2026Article
- Somatic Kitl promotes mTOR to facilitate prophase I of meiosis in female embryonic gonads.Cell death & disease · 2025Article
- MEIOC prevents continued mitotic cycling and promotes meiotic entry during mouse oogenesis.bioRxiv : the preprint server for biology · 2025Article
- Reduced ALDH1A1 expression in multiple myeloma cells increases resistance to daratumumab via downregulation of retinoic acid.Cellular and molecular life sciences : CMLS · 2025Article
- Evolving Lessons on Metazoan Primordial Germ Cells in Diversity and Development.Molecular reproduction and development · 2025Review
- BMP and STRA8 act collaboratively to ensure correct mitotic-to-meiotic transition in the fetal mouse ovary.Development (Cambridge, England) · 2025Article
- AOP Report: Decreased ALDH1A (RALDH) activity leading to decreased fertility via disrupted meiotic initiation of fetal oogonia.Current research in toxicology · 2025Article
- The role of ALDH1A1 in glioblastoma proliferation and invasion.Chemico-biological interactions · 2024Article
- Tubular insulin-induced gene 1 deficiency promotes NADEMBO molecular medicine · 2024Article
- Juvenile hormones direct primordial germ cell migration to the embryonic gonad.Current biology : CB · 2024Article
- Neonatal vitamin A supplementation improves sheep fertility potential.Frontiers in veterinary science · 2024Article
- Using Embryo Models to Understand the Development and Progression of Embryonic Lineages: A Focus on Primordial Germ Cell Development.Cells, tissues, organs · 2024Review
- STRA8-RB interaction is required for timely entry of meiosis in mouse female germ cells.Nature communications · 2023Article
- Cell cycle regulation for meiosis in mammalian germ cells.The Journal of reproduction and development · 2023Review
- RA-RAR signaling promotes mouse vaginal opening through increasing β-catenin expression and vaginal epithelial cell apoptosis.Reproductive biology and endocrinology : RB&E · 2023Article
- The Beginning of Meiosis in Mammalian Female Germ Cells: A Never-Ending Story of Intrinsic and Extrinsic Factors.International journal of molecular sciences · 2022Review
- Deciphering Sex-Specific Differentiation of Human Fetal Gonads: Insight From Experimental Models.Frontiers in cell and developmental biology · 2022Review
- AOP Key Event Relationship report: Linking decreased retinoic acid levels with disrupted meiosis in developing oocytes.Current research in toxicology · 2022Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Substantial evidence exists that during fetal ovarian development in mammals, retinoic acid (RA) induces germ cells to express the pre-meiotic marker Stra8 and enter meiosis, and that these effects are prevented in the fetal testis by the RA-degrading P450 enzyme CYP26B1. Nonetheless, the role of RA has been disputed principally because germ cells in embryos lacking two major RA-synthesizing enzymes, ALDH1A2 and ALDH1A3, remain able to enter meiosis. Here we show that a third RA-synthesizing enzyme, ALDH1A1, is expressed in fetal ovaries, providing a likely source of RA in the absence of ALDH1A2 and ALDH1A3. In ovaries lacking ALDH1A1, the onset of germ cell meiosis is delayed. Our data resolve the conundrum posed by conflicting published data sets and reconfirm the model that meiosis is triggered by endogenous RA in the developing ovary.
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Registered trials
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.