WIKIMEDIA, RAMAEmbryonic deletion of a core circadian clock gene, Bmal1, leads to problems associated with accelerated aging in adult mice, including neurodegeneration, poor hair growth, eye and bone pathologies, and a decreased lifespan. Yet mice in which the gene is knocked out after birth don’t exhibit many of these aging-related phenotypes, according to a study published today (February 4) in Science Translational Medicine. The results suggest that the circadian clock gene plays different roles during embryogenesis and after birth.
“This is a thorough and well-conducted study,” said Ghislain Breton, who studies the circadian system at the University of Texas Health Science Center in Houston, but was not involved in the work. “The lesser phenotype when you disrupt Bmal1 after birth is very intriguing,” he continued. “It means that certain early developmental stages are likely more sensitive to circadian clock disruptions compared to adulthood.”
“What is really important about this work is that the longevity is normal in the [postnatal Bmal1 knockout] mice,” said Marina Antoch, a professor of oncology at the Roswell Park Cancer Institute in Buffalo, New York, who was not involved in the research.
Circadian clocks regulate the physiology and behavior of many organisms. Disruption of key circadian clock regulators is known ...
