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Ptk2b deletion improves mice folliculogenesis and fecundity via inhibiting follicle loss mediated by Erk pathway
Author(s) -
Cong Yanyan,
Wu Haibo,
Bian Xuejiao,
Xie Qin,
Lyu Qifeng,
Cui Junqi,
Suo Lun,
Kuang Yanping
Publication year - 2021
Publication title -
journal of cellular physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.529
H-Index - 174
eISSN - 1097-4652
pISSN - 0021-9541
DOI - 10.1002/jcp.29914
Subject(s) - folliculogenesis , biology , follicle , oocyte , microbiology and biotechnology , ovarian follicle , zona pellucida , mapk/erk pathway , doublesex , medicine , andrology , endocrinology , oogenesis , ovary , signal transduction , embryo , genetics , embryogenesis , rna , gene , rna splicing
Ptk2b has been found playing critical roles in oocyte maturation and subsequent fertilization in vitro. But what is the exact in vivo function in reproduction still elusive. Here, by constructing Ptk2b mutant mice, we found Ptk2b was not essential for mice fertility, unexpectedly, contrary to previously reported in vitro findings, we found Ptk2b ablation significantly improved female fecundity. Follicle counting indicated that the number of primordial follicles and growing follicles in matured mice was significantly increased in the absence of Ptk2b , whereas the primordial follicle formation showed no defects. We also found this regulation was in an autophosphorylation independent pathway, as autophosphorylation site mutant mice (PTK2B Y402F ) show no phenotype in female fertility. Further biochemistry studies revealed that Ptk2b ablation promotes folliculogenesis via Erk pathway mediate follicle survival. Together, we found a novel biological function of Ptk2b in folliculogenesis, which could be potentially used as a therapeutic target for corresponding infertility.