A trans-Atlantic dispute has formed between two camps of researchers pursuing a gene that could lead to drugs that enhance longevity. British scientists say the longevity gene is “nearing the end of its life,” but the Americans whose work is under attack say the approach remains as promising as ever.

The dispute concerns genes that make sirtuins, proteins involved in controlling cells’ metabolism. Because of their metabolic role, the sirtuins may mediate the 40-percent-longer life enjoyed by laboratory rats and mice put on a very low-calorie diet.

People cannot keep to such a low-fat diet, but drugs that activate sirtuin would in principle be a painless way for humans to add years of lean and healthy life. This idea took wing when resveratrol, a substance found in trace quantities in red wine, was reported to activate sirtuin. In 2008 GlaxoSmithKline, the pharmaceutical company, paid $720 million for Sirtris, a startup company trying to develop resveratrol-mimicking drugs that activate sirtuins.

Since then, several aspects of the sirtuin story have come under scientific challenge, including doubts as to whether resveratrol’s effects are really exercised through sirtuin, and whether the sirtuins are the real or only mediators of the longevity increase linked to a low-calorie diet.

Despite these concerns, the idea that sirtuins promote longevity appeals to scientists because of experiments that were started in yeast and repeated in two other standard laboratory organisms, the roundworm and the fruit fly.

It is these foundation experiments that have now come under attack by David Gems and Linda Partridge, researchers on aging at University College London. In an article published Wednesday in the journal Nature, they and colleagues have reexamined experiments in which roundworms and flies, genetically manipulated to produce more sirtuin than normal, were reported to live longer.

Both experiments were flawed, they say, because the worms and flies used as a control were not genetically identical to the test organisms. The London researchers report that they have repeated the experiments with proper controls and found that extra sirtuin does not, after all, make the worms or flies live longer.

In the worm experiment, published by Leonard Guarente of the Massachusetts Institute of Technology in 2001, the strain of worms used had picked up an extra mutation which also had the effect of prolonging life, the London researchers report. When the mutated gene is removed, the worms with extra sirtuin do not live longer, they said.

Guarente said he did not agree with the thrust of this criticism. The 2001 experiment was done with the best techniques then available, he said. When he heard of the mutated gene two years ago, he redid the experiment, using worms from which the gene had been removed. The worms with extra sirtuin still lived longer, although the effect was less pronounced than before, a finding he also reports in the current Nature.

“We agree there is a glitch in one of the worm strains used in the 2001 paper,” Guarente said in an interview. “We absolutely do not agree that there is a serious question about whether sir2 extends life span in worms,” he said, using the name for the worm’s version of the sirtuin protein.

“I think the whole thing is a tempest in a teapot,” he said.

Stephen Helfand of Brown University is the author of the fly experiments. Like Guarente, Helfand criticized the London researchers for focusing on an old experiment of his and ignoring a subsequent one that reached the same conclusion with a much-improved technique.