In a discovery that could help determine what causes early-onset puberty in females, a team of researchers from Oregon Healthy and Science University and the University of Pittsburgh have for the first time discovered the genes responsible for triggering the process.

According to medical experts, puberty typically begins around ages 10 or 11 for girls and around age 12 for boys, though it can start earlier or later based on an individual. Now, as the authors of the new study report in the latest edition of the journal Nature Communications, they have found new insight into just how the process of sexual development is controlled by the brain.

The key is an elaborate supergroup of genes known as the Zinc finger (ZNF) family, a group of about 800 individual genes that OHSU neuroscientist Dr. Alejandro Lomniczi and his colleagues have found are responsible for regulating puberty’s timing in advanced nonhuman primates.

Some of these genes, they explained, operate within the neuroendocrine brain and act as a sort of “neurobiological brake”—delaying the activation of the hypothalamic genes that kickstart puberty until the end of childhood. Typically, this prevents puberty from starting prematurely.

Experiments successfully delayed puberty in female rats

As Dr. Lomnicizi’s team explained in their research, the ZNF gene family encodes repressors (proteins which inhibits gene expression) to suppress the launch of puberty. Knowing this can enable them to determine what environmental factors are involved in precocious or early onset puberty, which has been linked to a number of cancers and other health issues.

“Deepening our understanding of how the brain controls the initiation of puberty will allow us to understand why girls are initiating puberty at much earlier ages,” Dr. Lomniczi said Wednesday in a statement. “This knowledge may help build a foundation for developing new avenues to treat precocious puberty. Our suspicion, is that chemical substances contained in man-made products and other environmental factors, such as nutrition, may accelerate reproductive development by epigenetically antagonizing gene repressors such as ZNFs.”

ZNFs work through the activation of mechanisms that can modify the activity of a gene without altering the sequence of DNA, he and his fellow researchers explained. For this reason, the ZNFs are considered to act “epigenetically,” which means that they communicate environmental data to a person’s genes without actually altering their genetic code in any way.

They found that the abundance of some ZNFs, including messenger RNAs encoding GATAD1 and ZNF573, decreases during the transitional stage before puberty in nonhuman primates, when the so-called neurological brake is released and the hypothalamic genes are begin the process are released. They found that by increasing the amount of GATAD1 or ZNF573 in the hypothalamus of prepubescent female rates, they could delay puberty’s onset in these rodents.

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Feature Image: Thinkstock

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