Highly expressed in the testis, a gene named Ranbp9 has been found to play a critical role in male fertility by controlling the correct expression of thousands of genes required for successful sperm production. A group of researchers led by Professor Wei Yan, at the University of Nevada School of Medicine has discovered that a loss of function of Ranbp9 leads to severely reduced male fertility due to disruptions in sperm development. A paper reporting this finding was published in PLOS Genetics on December 4, 2014.
Male infertility affects 1 out of 20 men of reproductive age worldwide and the underlying causes remain largely unknown. The production of functional sperm is a prerequisite for male fertility, and is achieved through a complex process termed spermatogenesis, which is controlled by numerous genes that are synthesized and processed into messenger ribonucleic acid (mRNA) molecules of different sizes. Disruptions of mRNA processing would lead to aberrant mRNA contents in the developing male germ cells, failed sperm production, and male infertility.
The published study demonstrates that Ranbp9 acts to control the correct processing of mRNA molecules after their syntheses from thousands of genes involved in sperm production. This finding places Ranbp9 as a master regulator of sperm production. Thus, interference of this gene may provide novel diagnostics and therapeutics for male infertility patients, as well as the development of male non-hormonal contraceptives.
All works published in PLOS Genetics are open access, which means that everything is immediately and freely available.
Citation: Bao J, Tang C, Li J, Zhang Y, Bhetwal BP, et al. (2014) RAN-Binding Protein 9 Is Involved in Alternative Splicing and Is Critical for Male Germ Cell Development and Male Fertility. PLoS Genet 10(12): e1004825. doi:10.1371/journal.pgen.1004825
Funding: This work was supported by grants from the NIH (HD060858, HD071736 and HD074573 to WY). All transgenic mouse lines were generated and/or maintained in the University of Nevada Genetic Engineering Center (UNGEC) supported by a NIH COBRE grant (P20-RR18751). The Flow Cytometry and Proteomic analyses described here were supported by a grant from the National Institute of General Medical Sciences (8P20GM10344011). The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.
Competing Interests: The authors have declared that no competing interests exist.