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To find out, they cloned T1R1-T1R3 receptors from a variety of songbirds and tested their responses to sugar.
All the receptors they tested―from birds with sugar-rich and sugar-poor diets alike―interacted strongly with sugar molecules.
This confirmed that, as with hummingbirds, songbirds regained perception of sweetness via mutations of the gene for T1R1 and T1R3.
By contrast, umami receptors cloned from the Tyranni, a sister group to the Passeri, did not interact with sugars, though they did so strongly with amino acids typical of meat.
The mutations in the songbird lineage must thus have happened after the Passeri and Tyranni lines diverged, but before the Passeri themselves began proliferating into their current variety.
Intriguingly, when Dr Toda and Dr Baldwin looked at the molecular modifications which allowed the T1R1-T1R3 receptors of hummingbirds and Passeri to detect sweetness, they found them to be completely different.
Both, though, involved numerous changes to the underlying DNA, suggesting a strong evolutionary pressure to optimise them.
This pressure was probably a consequence of competition to fill the new ecological niches opened up by an ability to recognise sweet things as both edible and nutritious.
为了找到答案,他们从各种鸣禽中克隆了T1R1-T1R3受体,并测试了它们对糖的反应。
他们测试的所有受体――来自高糖和低糖饮食的鸟类――都与糖分子发生了强烈的相互作用。
该研究证实,鸣禽和蜂鸟一样,通过T1R1和T1R3基因的突变重新获得了对甜味的感知。


有趣的是,户田博士和鲍德温博士研究了使蜂鸟和雀形目的T1R1-T1R3受体感知甜味的分子修饰,结果发现它们是完全不同的。
然而,这两种方法都涉及到基础DNA的大量变化,这表明有强大的进化压力来优化它们。
这种压力很可能是人类为了填补新的生态位而展开竞争的结果,这种生态位是人类识别甜味食物既可食用又有营养的能力所开启的。
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