Researchers are delving into abnormal gene function in mitochondria, structures within cells that power our lives. Mitochondria are the place where energy is generated from the most basic molecules of food. Because this function is essential to life, defects in mitochondria may affect a wide range of organ systems in humans and animals.

Mice with a defective mitochondrial protein called MCLK1 produce elevated amounts of reactive oxygen when young; that should spell disaster, yet according to a study in this week's JBC these mice actually age at a slower rate and live longer than normal mice.

Mitochondria are the powerhouses of cells. Underneath their smooth surface they harbor an elaborately folded inner membrane. It holds a multitude of bottleneck like invaginations, which expand into elongated cavities (cristae). The narrow shape of the entrance or pore to the cristae ('crista junction') allows separation of the intracristal space and storage of molecules.

Cells are filled with membrane-bound organelles like the nucleus, mitochondria and endoplasmic reticula. Over the years, scientists have made much progress in understanding the biomolecular details of how these organelles function within cells, but understanding the actual physical forces that maintain the structures of these organelles' membranes continues to be a challenge.

A new study by Narendra et al. suggests that Parkin, the product of the Parkinson's disease-related gene Park2, prompts neuronal survival by clearing the cell of its damaged mitochondria.

A study in the Sept. 21 on-line edition of Nature Medicine describes the function and interaction of a critical molecule involved in cell death in Alzheimer’s disease patients.

Researchers report on a previously unknown relationship between stem cell potency and the metabolic rate of their mitochondria –a cell's energy makers. Stem cells with more active mitochondria also have a greater capacity to differentiate and are more likely to form tumors.

Imagine trying to figure out how your car's power train works from just a few of its myriad components: It would be nearly impossible. Scientists have long faced a similar challenge in understanding cells' tiny powerhouses — called "mitochondria" — from scant knowledge of their molecular parts.

Scientists have determined that human cells are able to shift important gene products into their own mitochondria, considered the power plants of cells. The finding could eventually lead to therapies for dozens of diseases.

A process of self-digestion called autophagy prompts the maturation of red blood cells. Without a protein called Nix, the cells would not effectively rid themselves of organelles called mitochondria and consequently become short-lived, leading to anemia, said researchers at Baylor College of Medicine in Houston in a report that appears online today in the journal Nature.

As the major source of free radicals in cells, mitochondria contribute to the high levels of oxidative stress believed to play a role in the pathogenesis of Alzheimer’s disease.

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