Subcellular chatter regulates longevity

May 19, 2020

As people get older, they often feel less energetic, mobile or active. This may be due in part to a decline in mitochondria, the tiny powerhouses inside of our cells, which provide energy and regulate metabolism. In fact, mitochondria decline with age not only in humans, but in many species. Why they do so is not well understood. Scientists at the Max Planck Institute for Biology of Ageing in Cologne set out to understand how mitochondrial function is diminished with age and to find factors that prevent this process. They found that communication between mitochondria and other parts of the cell plays a key role.

For their studies, the scientists used the simple roundworm, Caenorhabditis elegans, an important model system for ageing research. Over half the genes of this animal are similar to those found in humans, and their mitochondria also decline with age. From their research, the scientists found a nuclear protein called NFYB-1 that switches on and off genes affecting mitochondrial activity, and which itself goes down during ageing. In mutant worms lacking this protein, mitochondria don't work as well and worms don't live as long.

Unexpectedly, the scientists discovered that NFYB-1 steers the activity of mitochondria through another part of the cell called the lysosome, a place where basic molecules are broken down and recycled as nutrients. "We think the lysosome talks with the mitochondria through special fats called cardiolipins and ceramides, which are essential to mitochondrial activity," says Max Planck Director, Adam Antebi, whose laboratory spearheaded the study. Remarkably, simply feeding the NFYB-1 mutant worms cardiolipin restored mitochondrial function and worm health in these strains.

Because cardiolipins and ceramides are also essential for human mitochondria, this may mean human health and ageing can be improved by understanding on how such molecules facilitate communication between different parts of the cell. This work has been recently published in Nature Metabolism.
-end-
Original publication

Rebecca George Tharyan, Andrea Annibal, Isabelle Schiffer, Raymond Laboy, Ilian Atanassov, Anna Luise Weber, Birgit Gerisch and Adam Antebi

NFYB-1 regulates mitochondrial function and longevity via lysosomal prosaposin. Nature Metabolism; May 18, 2020

Max-Planck-Gesellschaft

Related Mitochondria Articles from Brightsurf:

Researchers improve neuronal reprogramming by manipulating mitochondria
Researchers at Helmholtz Zentrum M√ľnchen and Ludwig Maximilians University Munich (LMU) have identified a hurdle towards an efficient conversion: the cell metabolism.

Inside mitochondria and their fascinating genome
EPFL scientists have observed -- for the first time in living cells -- the way mitochondria distribute their transcriptome throughout the cell, and it involves RNA granules that turn out to be highly fluid.

'Cheater mitochondria' may profit from cellular stress coping mechanisms
Cheating mitochondria may take advantage of cellular mechanisms for coping with food scarcity in a simple worm to persist, even though this can reduce the worm's wellbeing.

A ribosome odyssey in mitochondria
The ciliate mitoribosome structure provides new insights into the diversity of translation and its evolution.

Fireflies shed light on the function of mitochondria
By making mice bioluminescent, EPFL scientists have found a way to monitor the activity of mitochondria in living organisms.

First successful delivery of mitochondria to liver cells in animals
This experiment marks the first time researchers have ever successfully introduced mitochondria into specific cells in living animals.

Lack of mitochondria causes severe disease in children
Researchers at Karolinska Institutet in Sweden have discovered that excessive degradation of the power plants of our cells plays an important role in the onset of mitochondrial disease in children.

Unexpected insights into the dynamic structure of mitochondria
As power plants and energy stores, mitochondria are essential components of almost all cells in plants, fungi and animals.

Mitochondria are the 'canary in the coal mine' for cellular stress
Mitochondria, tiny structures present in most cells, are known for their energy-generating machinery.

Master regulator in mitochondria is critical for muscle function and repair
New study identifies how loss of mitochondrial protein MICU1 disrupts calcium balance and causes muscle atrophy and weakness.

Read More: Mitochondria News and Mitochondria Current Events
Brightsurf.com is a participant in the Amazon Services LLC Associates Program, an affiliate advertising program designed to provide a means for sites to earn advertising fees by advertising and linking to Amazon.com.