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【bio-news】早期哺乳动物丢失的基因是否具有夜视

http://www.eurekalert.org/pub_releases/2006-10/uom-dmg101106.php
Does missing gene point to nocturnal existence for early mammals?
A gene that makes cells in the eye receptive to light is missing in humans, researchers have discovered.

They say that whereas some animals like birds, fish and amphibians have two versions of this photoreceptor, mammals, including humans, only have one.

The findings ?published in the Public Library of Science journal PLoS Biology ?reveal how our experience of the light environment may be impoverished compared to other vertebrates and fits with the suggestion that early mammals were at one time wholly nocturnal creatures.

"The classical view of how the eye sees is through photoreceptive cells in the retina called rods and cones," explained Dr Jim Bellingham, who led the research at The University of Manchester.

"But, recently, a third photoreceptor was discovered that is activated by a gene called melanopsin. This melanopsin photoreceptor is not linked to sight but uses light for non-visual processes, such as regulating our day-night rhythms and pupil constriction."

Although the melanopsin gene is present in all vertebrates, the version in mammals was unusually different to that found in fish, amphibians and birds.

"At first, we put this genetic anomaly between mammals and other vertebrates down to evolutionary differences," said Dr Bellingham, who is based in the Faculty of Life Sciences.

"But we have now learnt that other vertebrates have a second melanopsin gene ?one that matches the one found earlier in mammals and humans. The first melanopsin gene found in the other classes of vertebrates does not exist in mammals."

It is not yet clear how the functions of the two melanopsins differ but having different cone genes or 'opsins' allows vertebrates to detect different wavelengths of light and allows them to see colour.

The Manchester team now hopes to find out whether the two melanopsin genes in non-mammals play similar or different roles in non-visual light detection and so provide clues as to the implications of only having one melanopsin gene.

"The two genes and their associated proteins have been maintained in vertebrates for hundreds of millions of years, only for one of them to be lost in mammals.

"We are keen to discover why this might have happened ?perhaps the early mammals were at one stage nocturnal and had no need for the second gene, for instance. We also want to find out what losing one of these genes means for humans."

### 以前的常识是:
人,猴有红蓝绿三种细胞
非哺乳动物有四种,能看紫外

不知这篇有什么突破。 好,支持一下,此文章我已认领,如果24小时后没有完成,请其他战友自由认领。谢谢,偶得第201贴,加油!学习格瓦拉!为理想献身! 此文章我已认领,如果48小时后没有完成,请其他战友自由认领。 Does missing gene point to nocturnal existence for early mammals?丢失的基因帮助早期哺乳动物夜间生存?
A gene that makes cells in the eye receptive to light is missing in humans, researchers have discovered.研究者发现使人类细胞能感受光的一个基因丢失了。
They say that whereas some animals like birds, fish and amphibians have two versions of this photoreceptor, mammals, including humans, only have one.他们说像鸟、鱼、和两栖动物等一些动物有两种这样光感受器,然而包括人类在内的哺乳动物只有一种。
The findings ?published in the Public Library of Science journal PLoS Biology ?reveal how our experience of the light environment may be impoverished compared to other vertebrates and fits with the suggestion that early mammals were at one time wholly nocturnal creatures.这些发现发表在科学公共图书杂志上。生物学揭示了和其他脊椎动物相比,我们对光环境的体验如何可能被竭尽,这和早期哺乳动物曾经一度完全是夜间活动生物的现象吻合。
"The classical view of how the eye sees is through photoreceptive cells in the retina called rods and cones," explained Dr Jim Bellingham, who led the research at The University of Manchester. "But, recently, a third photoreceptor was discovered that is activated by a gene called melanopsin. This melanopsin photoreceptor is not linked to sight but uses light for non-visual processes, such as regulating our day-night rhythms and pupil constriction." “传统的观点认为眼睛是通过位于视网膜的称柱状细胞和锥体细胞的光感受细胞来视物的” 在曼彻斯特大学领导这项研究的Dr Jim Bellingham博士解释道,“但是,目前,第三种光感受器被发现了,它被一个叫黑视蛋白的基因激活。黑视蛋白光感受器与视力无关,但利用光线进行非视觉过程,例如调节我们的日夜节律和瞳孔收缩。”

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作者:admin@医学,生命科学    2011-02-17 18:02
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