LSM14B coordinates protein component expression in the P-body and controls oocyte maturation  

作　　者：Huiru Zhang Tao Zhang Xiang Wan Chang Chen Shu Wang Dongdong Qin Lufan Li Luping Yu Xin Wu 

机构地区：[1]State Key Laboratory of Reproductive Medicine and Offspring Health,Nanjing Medical University,Nanjing,Jiangsu 210029,China [2]Center for Reproductive Medicine and Obstetrics and Gynecology,Nanjing Drum Tower Hospital,Nanjing University Medical School,Nanjing,Jiangsu 210029,China

出　　处：《Journal of Genetics and Genomics》2024年第1期48-60,共13页遗传学报（英文版）

基　　金：supported by the National Key R&D Program of China(2021YFC2700201 to X.W.);the National Natural Science Foundation of China(32070831,32270897 to X.W.).

摘　　要：The generation of mature and healthy oocytes is the most critical event in the entire female reproductive process,and the mechanisms regulating this process remain to be studied.Here,we demonstrate that Smith-like(LSM)family member 14B(LSM14B)regulates oocyte maturation,and the loss of LSM14B in mouse ovaries leads to abnormal oocyte MII arrest and female infertility.Next,we find the aberrant transcriptional activation,indicated by abnormal non-surrounded nucleolus and surrounded nucleolus oocyte proportions,and abnormal chromosome assembly and segregation in Lsm14b-deficient mouse oocytes.The global transcriptome analysis suggests that many transcripts involved in cytoplasmic processing body(P-body)function are altered in Lsm14b-deficient mouse oocytes.Deletion of Lsm14b results in the expression and/or localization changes of P-body components(such as LSM14A,DCP1A,and 4E-T).Notably,DDX6,a key component of the P-body,is downregulated and accumulates in the nuclei in Lsm14b-deficient mouse oocytes.Taken together,our data suggest that LSM14B links mouse oocyte maturation to female fertility through the regulation of the P-body.

关 键 词：LSM14B P-BODY DDX6 MIl arrest Chromatin configuration 

分 类 号：R968[医药卫生—药理学]