Scientists Solve White Tiger Mystery

"The white tiger represents part of the natural genetic diversity of the tiger that is worth conserving, but is now seen only in captivity," says Shu-Jin Luo of China's Peking University.

Luo, Xiao Xu, Ruiqiang Li, and their colleagues advocate a proper captive management program to maintain a healthy Bengal tiger population including both white and orange tigers. They say it might even be worth considering the reintroduction of white tigers into their wild habitat.

The researchers mapped the genomes of a family of 16 tigers living in Chimelong Safari Park, including both white and orange individuals. They then sequenced the whole genomes of each of the three parents in the family.

Those genetic analyses led them to a pigment gene, called SLC45A2, which had already been associated with light coloration in modern Europeans and in other animals, including horses, chickens, and fish. The variant found in the white tiger primarily inhibits the synthesis of red and yellow pigments but has little to no effect on black, which explains why white tigers still show characteristic dark stripes.

Historical records of white tigers on the Indian subcontinent date back to the 1500s, Luo notes, but the last known free-ranging white tiger was shot in 1958. That many white tigers were hunted as mature adults suggests that they were fit to live in the wild. It's worth considering that tigers' chief prey species, such as deer, are likely colorblind.

Captive white tigers sometimes do show abnormalities, such as crossed eyes, but Luo says any frailties are likely the responsibility of humans, who have inbred the rare tigers in captivity. With the causal gene identified, the researchers ultimately hope to explore the evolutionary forces that have maintained tigers in both orange and white varieties.

Source-Eurekalert

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A Step to Unlocking Mystery of Ageing Taken By Swiss Researchers

by Rukmani Krishna on? May 25, 2013 at 11:28 PM Genetics & Stem Cells News A step closer to unlocking the mystery of ageing was taken by Swiss researchers after discovering the impact of a longevity gene in mice and then managing to extend the life-span of worms by 60 percent thanks to a basic antibiotic treatment.
"They were not only living longer, but were also more fit," said Johan Auwerx ion a video released by the Ecole Polytechnique Federale de Lausanne (EPFL), a cutting-edge Swiss research institute.

The findings of Auwerx's team have been published in the scientific journal Nature.

The goal of the research was to work out why certain individuals of the same species can have a far longer life-span than others.

"Our lab has for some time been using a complex genetic reference population of mice, which mimic the human population, to study ageing," said Auwerx.

The scientists started by examining mice's mitochondria -- a cell's version of a power plant -- and uncovered a group of three genes that affected the animals' life-span via their speed of functioning.

Those whose genes were 50 percent slower lived some 250 days longer, or about 30 percent of a mouse's lifetime.

"Based on this observation, we switched model, and started validating this experimentally in a worm," said Auwerx.

"Knocking down the same proteins, we could see an up to 60 percent extension of worm life-span," he added.

Auwerx underlined that since mitochondria are bacteria living within cells, his team then experimented with antibiotics, which target bacteria.

"We could see that treating the worms with the antibiotics also mimicked the genetic effects, and they also lived 60 percent longer," from 19 days to 30, he explained.

Mitochondria transform nutrients into various kinds of protein, and several previous studies have suggested that they may be the motor of ageing.

The Swiss team, working with counterparts in the Netherlands and United States, managed to identify the specific gene involved in the process and work out how variations in protein could affect life-span.

They worked out that so-called MRPs -- for mitochondrial ribosomal proteins -- had an inversely proportional impact on longevity.

In addition, they found that a lack of MRPs at key moments of an individual's early development caused stress on mitochondria.

This has short-term negative impacts such as a fall in fertility, but in the long term appeared to result in a better muscle structure as well as a longer life.

The researchers underlined that further studies would be needed to confirm whether antibiotics could be used to rein in ageing in mammals.

Source-AFP

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