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Our study found that <jats:italic>Dcaf2<\/jats:italic> was expressed in mouse spermatogonia and spermatocyte. The depletion of <jats:italic>Dcaf2<\/jats:italic> in germ cells by crossing <jats:italic>Dcaf2<\/jats:italic><jats:sup><jats:italic>fl\/fl<\/jats:italic><\/jats:sup> mice with stimulated by retinoic acid gene 8(<jats:italic>Stra8)<\/jats:italic>\u2010Cre mice caused a reduction in progenitor spermatogonia and differentiating spermatogonia, eventually leading to the failure of meiosis initiation and male infertility. Further studies showed that depletion of <jats:italic>Dcaf2<\/jats:italic> in germ cells caused abnormal accumulation of the substrate proteins, cyclin\u2010dependent kinase inhibitor 1A (p21) and thymine DNA glycosylase (TDG), decreasing of cell proliferation, increasing of DNA damage and apoptosis. Overexpression of p21 or TDG attenuates proliferation and increases DNA damage and apoptosis in GC\u20101 cells, which is exacerbated by co\u2010overexpression of p21 and TDG. The findings indicate that DCAF2 maintains the proliferation and differentiation of progenitor spermatogonia by targeting the substrate proteins p21 and TDG during the S phase.<\/jats:p>","DOI":"10.1111\/cpr.13676","type":"journal-article","created":{"date-parts":[[2024,6,5]],"date-time":"2024-06-05T04:45:54Z","timestamp":1717562754000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":8,"title":["<scp>DCAF2<\/scp> regulates the proliferation and differentiation of mouse progenitor spermatogonia by targeting p21 and thymine <scp>DNA<\/scp> glycosylase"],"prefix":"10.1111","volume":"57","author":[{"given":"Hongwei","family":"Wei","sequence":"first","affiliation":[{"name":"The Innovation Centre of Ministry of Education for Development and Diseases The second Affiliated Hospital, School of Medicine, South China University of Technology  Guangzhou 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