Deletion of the PDZ-binding kinase (Pbk) gene does not affect male fertility in mice

生物 激酶 附睾 蛋白激酶A 基因剔除小鼠 内科学 精子 男科 内分泌学 精子发生 细胞生物学 基因 遗传学 医学
作者
Yuka Miki,Lalitha Devi,Yuji Imai,Naojiro Minami,Tsuyoshi Koide,Sandeep Goel
出处
期刊:Reproduction, Fertility and Development [CSIRO Publishing]
卷期号:32 (10): 893-893 被引量:3
标识
DOI:10.1071/rd19445
摘要

The PDZ-binding kinase (PBK) protein is localised exclusively in spermatogenic cells, such as spermatogonia, spermatocytes and round spermatids, of the adult testis. However, its role in male fertility remains unknown. Analysis of adult Pbk-knockout (KO) male mice showed no significant difference in the weight of the testes, epididymis and seminal vesicle compared with adult wild-type (WT) mice. There were no significant differences in testis morphology, tubule diameter and the number of offspring born to females mated with KO or WT male mice. Sperm number, motility and morphology did not differ significantly between KO and WT mice. The oocyte fertilisation rate and embryo development following IVF were comparable between groups fertilised using spermatozoa from KO versus WT mice (P>0.05). Further analysis revealed that the phosphorylation of the mitogen-activated protein kinases (MAPKs) p38 kinase, c-Jun N-terminal kinase (JNK) and extracellular signal-regulated kinases was dysregulated in the testis of KO mice. In conclusion, Pbk-KO male mice are fertile and their spermatozoa and testis do not show any morphological and functional abnormalities despite the dysregulated phosphorylation of MAPKs. It is likely that functional redundancy of PBK and overlapping substrate specificities of the MAPK superfamily compensated for the loss of PBK from the testis.

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