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“We developed a method to detect proteins whose molecular evolution correlates with longevity of a species. The proteins we detected changed in a particular pattern, suggesting that evolution of these proteins was not by accident, but rather by design to cope with the biological processes impacted by ageing, such as DNA damage. The results suggest that long-lived animals were able to optimise bodily repair which will help them fend off the ageing process.”

Only microscopic amounts of DNA are left on the skeletons, including all the bacteria that lived on the animals. No usable DNA is therefore often found in bone, but mammoth hair is plentiful. Shampooed and bleached and digested, the hair, even at 18,000 years old, can have 90% of the DNA left. The genome shows 4 different "races" of this species. Research has also shown the recreated blood of mammoth. It doesn't decrease its oxygen capacity at the low temperatures the mammoth had to endure. That increased oxygen-offloading ability was one of the essential physiological changes evolved especially for this species, just like the Yuka kidney.

Cloning the mammoth has been an aim of Japanese scientists for several years. They discovered almost intact bone marrow from a thigh bone in Yakutsk and hope to use a female elephant for what is obviously more than a simple experiment within the next 5 years.

The study defined a new role for a protein called polynucleotide phosphorylase (PNPASE) in regulating the import of RNA into mitochondria. Reducing the expression--or output--of PNPASE decreased RNA import, which impaired the processing of mitochondrial genome-encoded RNAs. Reduced RNA processing inhibited the translation of proteins required to maintain the mitochondrial electron transport chain that consumes oxygen during cell respiration to produce energy. With reduced PNPASE, unprocessed mitochondrial-encoded RNAs accumulated, protein translation was inhibited, and energy production was compromised, leading to stalled cell growth.

Geng Wang developed a strategy to target and import specific RNA molecules encoded in the nucleus into the mitochondria and, once there, to express proteins needed to repair mitochondrial gene mutations.

First, the researchers had to find a way to stabilize the reparative RNA so that it was moved out of the nucleus and then localized to the mitochondrial outer membrane. This was accomplished by modifying an export sequence to direct the RNA to the mitochondrion. Once the RNA was in the area of the transport machinery on the mitochondrial surface, then a second transport sequence was required to direct the RNA into the targeted organelle. With these two modifications, a wide range of RNAs were targeted to and imported into the mitochondria, where they worked to repair defects in mitochondrial respiration and energy production in two different cell line models of human mitochondrial disease.