Female rattlesnakes double as long-term sperm banks

Female rattlesnakes double as long-term sperm banks

CHRIS JOHNS/NGS IN BRIEF Live longer with the same genes Snake stores sperm for five years before giving birth FAMILY planning campaigners looking f...

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CHRIS JOHNS/NGS

IN BRIEF Live longer with the same genes

Snake stores sperm for five years before giving birth FAMILY planning campaigners looking for a mascot should consider the eastern diamond-backed rattlesnake. A female of the species can store sperm in her body for at least five years before using it. The rattlesnake (Crotalus adamanteus) in question was collected in Florida in 2005 and kept in a private collection for five years, with no contact with other snakes. In late 2010, she unexpectedly gave birth to 19 snakelets. To find out what had happened, Warren Booth of North Carolina State University in Raleigh took samples of DNA from the mother and her young.

Booth studies “virgin birth”, in which a female produces young without any contribution from a male. But in this case the snakelets carried genes that their mother didn’t, so she must have mated before she was captured and stored the sperm (Biological Journal of the Linnean Society, DOI: 10.1111/j.1095-8312.2011.01782.x). Previous studies have hinted that reptiles can store sperm for several years, but this is the first case confirmed by genetics. Booth suspects other reptiles can store sperm even longer. “How long is anyone’s guess,” he says. It’s becoming clear that snakes have unconventional ways of reproducing, including virgin birth and long-term sperm storage, says William Holt of the Institute of Zoology in London, though so far no one knows how they do it.

The beaver that ate Yellowstone THE volcanic activity that shaped Yellowstone national park may have sculpted something on a much smaller scale too – the teeth of some rodents. Mountain beavers (Aplodontia rufa) have teeth with deep crowns, thick enamel and short roots – a condition called hypsodonty, typical of animals that chew gritty, silica-rich grasses. Yet they are partial to soft plants,

so why the tough teeth? Samantha Hopkins at the University of Oregon in Eugene looked at fossils of the beavers’ extinct relatives to find out, and discovered that the feature first appeared in north-west Nevada and Oregon 10 to 15 million years ago. At the time, vegetation there would have been frequently blanketed in volcanic dust from the Yellowstone hotspot and the

Columbia River Basalts. “All that silica-rich, lightweight, abrasive material implies lots of tooth abrasion,” says Hopkins, who presented her findings at the Geological Society of America’s annual meeting in Minneapolis, Minnesota, last week. Just 160 kilometres to the south, the rodents coped without hypsodont teeth. While there was volcanic activity from the Sierra Nevada mountains, it wasn’t as bad as in the north.

FOR the first time, chemical changes that increase lifespan have been shown to pass from one generation to the next with no alteration to the DNA code itself. Anne Brunet of Stanford University in California and colleagues modified a key protein in the roundworm Caenorhabditis elegans. The protein is part of the chromatin remodelling complex (CRC), which winds chromatin to reveal or conceal genes. This “epigenetic” modification altered the expression of genes linked to stress resistance, and increased the worms’ lifespan. Although the worms’ DNA was not altered, the changes affecting the CRC were inherited by their descendants, which also lived longer than usual (Nature, DOI: 10.1038/nature10572). Understanding how non-DNA markers are inherited could aid treatment for age-related diseases, Brunet suggests.

Youthful cure for sickle cell disease SWITCHING off a single gene could help treat sickle cell disease by keeping the blood forever young. The condition is caused by a mutant form of adult haemoglobin, but not by fetal haemoglobin. Stuart Orkin of Harvard Medical School in Boston, and colleagues, effectively cured mice that normally develop a sickle cell-like condition by knocking out BCL11A, the gene that controls the switchover from fetal to adult haemoglobin production (Science, DOI: 10.1126/ science.1211053). Gene therapy to block BCL11A in humans might provide similar benefits, but a drug that blocks the function of BCL11A would provide an easier and cheaper way to treat large populations, says Ortin. 22 October 2011 | NewScientist | 19