Yeast gene makes old cells young again

Yeast gene makes old cells young again

For new stories every day, visit newscientist.com/news Python genes get Yeast points way to making old cells young again frantic after meals CHILDREN...

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For new stories every day, visit newscientist.com/news

Python genes get Yeast points way to making old cells young again frantic after meals CHILDREN typically have the lifespan (Science, DOI: 10.1126/ they acquire clumps of proteins

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same life expectancy at birth, regardless of whether their father is 20 years old or 80. This must mean that the man’s reproductive cells somehow reset their clocks, but how they do this has been a mystery. Now a gene that reverses ageing effects in yeast is providing some clues. Under stressful conditions yeast cells forgo asexual reproduction and split into four spores, each containing half the chromosomes of a typical cell, like human eggs and sperm. As the cells get older,

and extra pieces of DNA, but when Angelika Amon at the Massachusetts Institute of Technology and colleagues tracked spores from old and young yeast cells they found that such abnormalities disappeared, meaning all spores had the same lifespan. Clumped protein seems to be cleared through autophagy, in which the cell “eats” itself. During sporulation, a gene called NDT80 was expressed. What’s more, switching on NDT80 in ageing cells doubled their

science.1204349). The closest relative of NDT80 in mammals is p53, a gene that regulates cell cycles. “We may have found a way to rejuvenate cells and erase ageing markers,” says Amon. The paper is “provocative”, says Michal Jazwinski at Tulane University in New Orleans, Louisiana: “People have attempted to examine what rejuvenates gametes for some time. It looks like NDT80 is playing an important role – it narrows down the territory to be examined.” andy sacks/stone/getty

A BURMESE python that has just eaten a goat may look like it’s resting, but on the inside it’s frantic. The python’s digestion switches on an unusually large number of genes. Pythons eat large meals very infrequently. To conserve energy between meals, they mothball their innards, substantially shrinking most of their internal organs. Then, after a meal, their intestines more than double in mass, and the heart and kidneys increase by half. This involves a huge amount of genetic turmoil. To find out just how much, Todd Castoe and colleagues at the University of Colorado at Denver measured gene activity in the organs of Burmese pythons, Python molurus bivittatus, before and immediately after meals. About 1800 dormant genes switched on within 24 hours of a meal, they reported last week at the Society for the Study of Evolution meeting in Norman, Oklahoma. Similar activation also occurs in the liver, kidney and intestines, they say. This is a staggering change: previously only a few dozen and up to a few hundred genes had been seen to change to cope with new conditions. Even the transition from an unfertilised egg to a 4-celled embryo – one of the biggest changes in an organism’s life – involves fewer than 3000 genes, a previous study has found.

Jet-setting worm has first-class DNA YOU would probably expect worms in California and France to have different genes, even within one species. Not so for a stretch of chromosome from the laboratory workhorse Caenorhabditis elegans. Joshua Shapiro of Princeton University and his colleagues compared about 40,000 genetic markers from 97 wild strains collected around the world. Those on chromosome 5 were virtually identical in the vast majority of worms, they reported last week at a meeting of the Society for the Study of Evolution in Norman, Oklahoma. Such a pattern can only be the result of strong natural selection for a gene, which would have caused all neighbouring genes to be selected as well. Based on the size of this “selective sweep”, Shapiro calculates that the favoured gene variant arose 100 to 200 years ago and has since spread across the world, most likely by hitch-hiking with human migrations. “This is the first time we have seen a natural selective sweep of this much DNA,” says Dee Denver at Oregon State University in Corvallis.

‘Broken’ toy shows infants’ rationality INFANTS can work out where the fault lies when a toy fails to work. Hyowon Gweon at Massachusetts Institute of Technology tested 16-month-olds’ reasoning using a toy that could be worked by pressing a button. Two adults showed an infant how to play with the toy, but both could make it work correctly just one time in two tries. They then passed the toy to the child – except that now, the button was no longer active. The infants appeared able to work out that the toy was faulty, given that both adults had previously had trouble making it work: 12 out of

17 infants soon turned to another toy. In a separate trial, one adult’s button presses always worked, while the second adult’s always failed. When the toy didn’t work for the infant, they appeared to reason they were doing something wrong, like the unsuccessful adult – 13 out of 19 children passed the toy to their parents for help (Science, DOI: 10.1126/science.1204493). Sara Cordes at Boston College in Massachusetts says the findings fit with current ideas about child cognition: “Infants are little adults when it comes to problem solving.”

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