ShanShan (2022-02-28 18:07):
#paper title: SKP1 drives the prophase I to metaphase I transition during male meiosis #link:https://pubmed.ncbi.nlm.nih.gov/32232159/ #doi:10.1126/sciadv.aaz2129  Sci Adv, 2020; 作者:该研究由美国宾夕法尼亚大学 Jeremy Wang 教授和武汉大学 罗孟成 教授合作完成(宾夕法尼亚大学博士后关永娟为第一作者)。 导读:研究发现SKP1位于减数分裂染色体联会区域,敲除SKP1导致雌雄小鼠均不育,粗线期染色体提前解离,无法进入减数分裂中期。进一步采用冈田酸处理,粗线期染色体仍然无法进入中期,这表明SKP1是减数分裂染色体获得进入中期能力所必须的一个调控因子。 研究亮点:①利用生殖细胞特异性Ddx4 cre 将SKP1敲除时发现雄性小鼠和雌性小鼠都不育; ②SKP1敲除小鼠模型是目前唯一一个具有提前解联会表型的小鼠模型
IF:11.700Q1 Science advances, 2020-03. DOI: 10.1126/sciadv.aaz2129 PMID: 32232159
SKP1 drives the prophase I to metaphase I transition during male meiosis
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Abstract:
The meiotic prophase I to metaphase I (PI/MI) transition requires chromosome desynapsis and metaphase competence acquisition. However, control of these major meiotic events is poorly understood. Here, we identify an essential role for SKP1, a core subunit of the SKP1-Cullin-F-box (SCF) ubiquitin E3 ligase, in the PI/MI transition. SKP1 localizes to synapsed chromosome axes and evicts HORMAD proteins from these regions in meiotic spermatocytes. SKP1-deficient spermatocytes display premature desynapsis, precocious pachytene exit, loss of PLK1 and BUB1 at centromeres, but persistence of HORMAD, γH2AX, RPA2, and MLH1 in diplonema. Strikingly, SKP1-deficient spermatocytes show sharply reduced MPF activity and fail to enter MI despite treatment with okadaic acid. SKP1-deficient oocytes exhibit desynapsis, chromosome misalignment, and progressive postnatal loss. Therefore, SKP1 maintains synapsis in meiosis of both sexes. Furthermore, our results support a model where SKP1 functions as the long-sought intrinsic metaphase competence factor to orchestrate MI entry during male meiosis.
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