Researchers have discovered a new pathway that promotes the activity of the cellular powerhouse, the mitochondria, during periods of stress; that could help protect against disease as we age. When our cells are impacted by stress, they halt protein production rather than create ones with mistakes. As that production stops, the mitochondria also change shape, becoming elongated. These findings, by scientists at The Scripps Research Institute, were
published in the journal Cell Reports.
"Just a couple hours of not making proteins [are] to be enough to remodel the mitochondria, and they can stay that way for hours," explained the senior author of the research Luke Wiseman, Ph.D., associate professor at TSRI. "That seems to be a protective way to promote mitochondrial function during the early stages of stress."
The Wiseman lab studies how stress in another organelle, the endoplasmic reticulum (ER), impacts the shape and function of mitochondria. One part of this relationship is the Unfolded Protein Response (learn about UPR from the video), and a signaling pathway called PERK. A reduction in PERK signaling can cause dysfunction in mitochondria during stressful periods, disrupting cellular function. However, overactivity in the pathway can cause the cell to self-destruct. In an aging cell, keeping those things in balance becomes difficult.
