South Middlesex Times

A recent study by a Rutgers University–New Brunswick researcher and colleagues has identified a genetic mutation in mice that affects cells necessary for sexual reproduction. This discovery may provide insights into male infertility and potentially lead to new treatments and contraceptives.

The research, led by Devanshi Jain, an assistant professor in the Department of Genetics at the School of Arts and Sciences, was published in Nature Communications. Jain's work focuses on understanding how germ cells develop into sperm, addressing key questions about reproductive cell development.

“We discovered that when mouse germ cells aren't properly connected to each other by intercellular bridges – links between cells that allow for communication and exchange of resources – they are unable to complete many of the processes necessary for development and survival, such as replicating their DNA and repairing DNA breaks,” said Jain.

In the United States, over 11% of men under 49 face infertility issues. While various factors contribute to this condition, deformities during meiosis—a process critical for creating sperm—are significant contributors. Jain’s lab is dedicated to identifying meiotic defects in mice.

Jain's findings contribute to ongoing research on reproductive defects, particularly focusing on how reproductive cells repair DNA damage. “Filling these knowledge gaps will help us understand the genetic basis of infertility, which we need to know to be able to come up with treatments, improve diagnoses, or even someday be able to successfully reproduce this developmental process in vitro,” she stated.

Future studies could potentially lead to the development of male contraceptives. “One day, men might be able to receive a small molecule that would deplete sperm but be reversible,” Jain suggested.

Researchers have recognized the importance of cell connectivity via intercellular bridges in sperm production. The TEX14 gene plays a role in forming these connections; its absence results in infertility due to failed meiosis.

Jain's research sheds light on previously unclear roles of intercellular bridges during meiosis. By comparing mice lacking functional TEX14 genes with those having partially depleted bridges due to a novel mutation, researchers were able to analyze bridge functions during meiosis.

“The collection of defects accumulated during meiosis in mice with defective intercellular bridges results in germ cell death, which leads to infertility. Our findings demonstrate that proper regulation of meiosis requires cell connectivity and establish a new framework for how we think about its control in the male germline,” explained Jain.

These findings enhance understanding of male infertility by elucidating complex cellular transitions leading up to sperm production. Other species also rely on similar connectivity methods during reproduction.

“Germ cell connectivity appears to be a critical part of germ cell development,” noted Jain. However, further research is needed before scientific challenges can be fully addressed.

“No one gene is going to solve male infertility; there are hundreds of genes involved in making meiosis happen properly,” concluded Jain. “This is just one more piece in a very complicated puzzle.”

Explore more ways Rutgers research is shaping the future.