|ZFIN ID: ZDB-PUB-180327-18|
An miR-200 cluster on chromosome 23 regulates sperm motility in zebrafish
Xiong, S., Ma, W., Jing, J., Zhang, J., Dan, C., Gui, J.F., Mei, J.
|Source:||Endocrinology 159(5): 1982-1991 (Journal)|
|Registered Authors:||Gui, Jian-Fang, Mei, Jie|
|PubMed:||29579206 Full text @ Endocrinology|
Xiong, S., Ma, W., Jing, J., Zhang, J., Dan, C., Gui, J.F., Mei, J. (2018) An miR-200 cluster on chromosome 23 regulates sperm motility in zebrafish. Endocrinology. 159(5):1982-1991.
ABSTRACTBesides its well-documented roles in cell proliferation, apoptosis and carcinogenesis, the function of p53-microRNA axis has been recently revealed in reproductive system. Recent studies indicated that miR-200 family members are dys-regulated in nonobstructive azoospermia patients, whereas their functions remain poorly documented. The aims of this study were to investigate the function of miR-200 family on zebrafish testis development and sperm activity. There was no significant difference in testis morphology and histology between wildtype and knockout zebrafish with deletion of miR-200 cluster on chromosome 6 (chr6-miR-200-KO) or on chromosome 23 (chr23-miR-200-KO). Interestingly, compared with wildtype zebrafish, the chr6-miR-200-KO zebrafish had no difference on sperm motility, while chr23-miR-200-KO zebrafish showed significantly improved sperm motility. Consistently, ectopic expression of miR-429a, miR-200a and miR-200b that are located in the miR-200 cluster on chromosome 23, significantly reduced motility traits of sperm. Several sperm motility-related genes, such as amh, wt1a and srd5a2b have been confirmed as direct targets of miR-200s on chr23. 17α-ethynylestradiol (EE2) exposure resulted in upregulated expression of p53 and miR-429a in testis and impairment of sperm motility. Strikingly, in p53 mutant zebrafish testis, the expression levels of miR-200s on chr23 were significantly reduced and accompanied by a stimulation of sperm motility. Moreover, the up-regulation of miR-429a associated with EE2 treatment was abolished in testis with p53 mutation. And the impairment of sperm activity by EE2 treatment was also eliminated when p53 was mutated. Together, our results reveal that miR-200 cluster on chromosome 23 controls sperm motility in a p53-dependent manner.