Mitochondria are cellular components that are responsible for manufacturing the energy needed to conduct essential activities inside the cell.    Andrew Dillin, from Howard Hughes Medical Institute (California, USA), and colleagues utilized the roundworm (Ceanorhabditis elegans) to show that modulation of the mitochondrial function in subsets of worm cells affect the longevity of the entire organism. The team engineered "transgenic" worms in which they disabled the gene known as cco-1, which normally  encodes a protein essential for biochemical reactions known collectively as the Electron Transport Chain (ETC), a necessary part of the energy-generating process of mitochondria.  Those worms with ETC selectively impaired by cco-1 loss in either intestine or nerve cells lived longer than normal worms, while worms with ETC perturbed in muscle, skin or the germline did not, suggesting that a unique signal emanating from damaged mitochondria in nerve or gut, and communicated at a distance, extended lifespan.  Further, the researchers then investigated the Unfolded Protein Response (UPR), mounted by cells when proteins accumulate excessively and begin to misfold, causing toxicity to cells.  In feeding  worms specific reagents that block the UPR, the team found that disruption of cco-1 in neurons or intestine no longer had a lifespan-enhancing effect. This dramatic finding illustrates that initiating refolding of proteins, in this case in response to faraway mitochondrial stress, is in fact the very activity that enhances longevity.  The researchers conclude that: “These results suggest that mitochondria may establish and perpetuate the rate of aging for the whole organism independent of cell-autonomous functions.”