Functional And Mechanism Study Of 1700121C10Rik On Male Reproduction

The mammalian sperm development and fertilization are very complicated,and the exact molecular mechanisms are far from clear.The deficiency of Prss54,a member of the testis specific serine protease family,led to sperm malformation,impaired sperm-zona pellucida penetration and male subfertility.Gene chip screening and quantitative RT-PCR verification revealed an almost complete absence of 1700121C10Rik RNAs in the testis of Prss54^-/-mice.The1700121C10Rik,located on chromosome 8C5,is a previously uncharacterized gene which consists of three exons,and its expression leads to two transcripts.Bioinformatics analysis and related experiments demonstrated that both transcripts of 1700121C10Rik belong to the class of lncRNAs.They are specifically expressed in the testicular tissue of adult male mice as revealed by tissue expression pattern analysis.In situ hybridization analysis revealed that 1700121C10Rik is predominantly expressed in round and elongating spermatids.Further experiments revealed that1700121C10Rik RNAs are located in both the cytoplasm and nucleus,and their expression coincides with the sexual maturity of mice.In light of these evidences,we hypothesized that1700121C10Rik plays an important role in the fertility of male mice.However,the loss of1700121C10Rik RNAs had no effect on the reproductive capability of male mice.We found that the testicular histology,sperm production,sperm morphology,sperm motility and acrosome reaction of sperm from 1700121C10Rik^-/-mice were not significantly different from those in the wt mice.Furthermore,the expression of Prss54 in the testis of 1700121C10Rik^-/-mice was not significantly different from that of wt mice,suggesting that PRSS54 may be an upstream regulator of 1700121C10Rik and participate in the regulation of its expression.To sum up,no obvious defects in the fertility of 1700121C10Rik^-/-male mice were detected.A lack of phenotype upon the absence of 1700121C10Rik RNAs could be attributed to functional redundancy or to compensatory mechanisms,and its exact role in male reproduction remains to be further studied in the future.