Understanding how neural stem cell activity is regulated and maintained has critical implications for regenerative approaches following brain trauma and disease. Now, researchers at the University of Cologne, led by Matteo Bergami, PhD, from the CECAD Cluster of Excellence for Aging Research, have discovered that the protein YME1L is essential in coordinating the shift between cellular proliferation and quiescence.

The article, “Metabolic control of adult neural stem cell self-renewal by the mitochondrial protease YME1L,” was published in Cell Reports.

“The transition between quiescence and activation in neural stem and progenitor cells (NSPCs) is coupled with reversible changes in energy metabolism with key implications for lifelong NSPC self-renewal and neurogenesis,” the researchers wrote. “How this metabolic plasticity is ensured between NSPC activity states is unclear. We find that a state-specific rewiring of the mitochondrial proteome by the i-AAA peptidase YME1L is required to preserve NSPC self-renewal.”

“Our results show that the activity of a single mitochondrial protease can significantly affect the fate of neural stem cells and the production rate of new nerve cells. These findings not only reveal a new layer of regulation in the biology of neural stem cells but may also have important implications for patients bearing mutated YME1L,” Bergami said.

“Together, our results reveal YME1L as playing a critical role in acutely shaping the mitochondrial proteome of NSPCs, adding an important layer of regulation in the mechanisms governing NSPC metabolic state transitions beyond potential changes in gene expression,” concluded the researchers.

Understanding how neural stem cell activity is regulated and maintained can help pave the way for new strategies following brain trauma and disease.

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