In a collaborative effort by the Oregon Healthy and Science University and the University of Pittsburgh, researchers identified the genes whose role is to trigger the onset of puberty, and manipulate them to delay puberty in female rats. They hope that the discovery will help determine exactly why causes early-onset puberty in females.
Medical literature holds that puberty begins around ages 10-11 for girls and around age 12 for boys, with variations on this from person to person. Now, the paper the OHSU team published in the journal Nature Communications allows us insight into how the brain fits into this complex process, controlling the sexual development of the body.
The biggest player in the process seems to be a supergroup of around 800 genes known as the Zinc finger (ZNF) family that neuroscientist Dr. Alejandro Lomniczi and his colleagues have found to be responsible for regulating the timing of puberty in advanced nonhuman primates. Some of these genes, they explain, function within the neoendocrine brain and work as “neurological brakes,” preventing puberty-related genes from activating during childhood.
The ZNF supergroup holds the blueprints for proteins that inhibit gene expression, allowing them to inhibit the onset of puberty. Knowing this allows Dr. Lomniczi’s team 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.”
The ZNF genes can modify genetic activity and expression without altering genetic information in any way, the researchers explain. They are thus considered to act “epigenetically,” meaning that they communicate environmental data to a person’s genes without any changes to DNA structure.
Dr. Lomniczi’s team found that the aboundance of some ZNF genes, including GATAD1- and ZND573-encoding RNA decrease during the transitional stage that precedes puberty in nonhuman primates — the time during which the “neurological brakes” are released and hypothalamic genes start activating. 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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