Physics. Researchers build quantum info bank by writing on the clouds.

Further investigation turned up 142 relatives, many of whom had low magnesium, hypertension, elevated blood cholesterol concentrations, or some combination of those problems. Even more intriguing, in all cases, the traits had been inherited from the individuals’ mothers—a clear indication that the gene at fault was located in the mitochondrial genome. The genes that Lifton has previously linked to low blood magnesium had all been nuclear. The mitochondrial location of the new gene mutation was a big advantage because that genome consists of only 16,000 base pairs as opposed to the 3 billion in the nuclear genome. Analysis of the mitochondrial genome of family members turned up one mutation found only in affected members and not detected in any of the thousands of mitochondrial genomes previously sequenced. This mutation altered one base—a thymidine was changed to a cytosine—in the gene for a mitochondrial transfer RNA (tRNA), which carries amino acids to the ribosome for protein synthesis. Because virtually all tRNAs have a thymidine at that spot, implying that it’s essential for the molecule’s function, the swap likely disrupts the tRNA’s structure and interferes with protein synthesis in the mitochondria. “The [thymidine] is extremely conserved,” says Carlos Moraes, an expert on mitochondrial genetics at the University of Miami, Florida. “That does indicate that the mutation could cause some kind of problem.” Moraes adds that he’s surprised that people with the mutation don’t suffer even more serious problems. Previous mutations found in mitochondrial tRNA genes have caused, among other things, muscle and nerve degeneration, although the extent of the damage can vary. A key question now is how the mutation produces hypertension and the other symptoms, which seem to be independent of one another. The low blood magnesium levels, which appear even in children, might be due to failure of the kidney to remove the mineral from the urine before it’s excreted— a process that requires a great deal of energy. In contrast, blood pressure and cholesterol concentrations were normal in young individuals but began increasing at about age 30. That suggests additional factors come into play with age. These might be environmental—say, a high-fat diet—or related to the declining mitochondrial function that some researchers think contributes to aging. Another crucial unknown is whether mitochondrial dysfunction contributes to metabolic syndrome in the general population. Kurtz thinks it might. “The implications are much greater than this finding in one family,” he predicts. –JEAN MARX