of Nebraska - Lincoln DigitalCommons@University of Nebraska - Lincoln Parental Care and Clutch Sizes in North and South American Birds Parental Care and Clutch Sizes in North and South American Birds
of Nebraska - Lincoln DigitalCommons@University of Nebraska - Lincoln Parental Care and Clutch Sizes in North and South American Birds Parental Care and Clutch Sizes in North and South American Birds
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内布拉斯加州 - 林肯 DigitalCommons@内布拉斯加大学 - 林肯 北美和南美鸟类的父母护理和离合器尺寸 北美和南美鸟类的父母护理和离合器尺寸
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通讯作者：
A. Cockburn
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作者：
V. Remeš;Beata Matysioková;A. Cockburn
热带和南半球地区小卵群的进化原因尚不清楚。亚历山大·斯库奇（Alexander Skutch）在50年前提出，南方较高的巢捕食率限制了父母向幼鸟提供食物的速度，从而通过限制父母可以喂养的幼鸟数量来限制蛋的数量。这一假说解释了不同纬度地区幼仔数量和亲代行为的差异，但尚未得到验证。这里，一项对亚利桑那州和阿根廷鸟类的详细研究表明，Skutch（cid:213）的假设解释了北美和南美的卵窝大小差异。然而，Skutch（cid:213）的假设和两个主要的替代方案都不能解释纬度之间的差异。秀丽隐杆线虫bcl -2样蛋白CED-9通过拮抗apaf -1样细胞死亡激活剂CED-4来防止程序性细胞死亡。内源性CED-9和CED-4蛋白定位于线粒体在野生型胚胎，其中大多数细胞存活。相反，在细胞被诱导死亡的胚胎中，CED-4呈现核周定位。细胞死亡激活剂EGL-1诱导的CED-4易位被ced-9的功能获得突变阻断，但不依赖于ced-3的功能，这表明CED-4易位先于CED-4易位
The evolutionary causes of small clutch sizes in tropical and Southern Hemisphere regions are poorly understood. Alexander Skutch proposed 50 years ago that higher nest predation in the south constrains the rate at which parent birds can deliver food to young and thereby constrains clutch size by limiting the number of young that parents can feed. This hypothesis for explaining differences in clutch size and parental behaviors between latitudes has remained untested. Here, a detailed study of bird species in Arizona and Argentina shows that Skutch(cid:213)s hypothesis explains clutch size variation within North and South America. However, neither Skutch(cid:213)s hypothesis nor two major alternatives explain differences between latitudes. The Caenorhabditis elegans Bcl-2—like protein CED-9 prevents programmed cell death by antagonizing the Apaf-1—like cell-death activator CED-4. Endogenous CED-9 and CED-4 proteins localized to mitochondria in wild-type embryos, in which most cells survive. By contrast, in embryos in which cells had been induced to die, CED-4 assumed a perinuclear localization. CED-4 translocation induced by the cell-death activator EGL-1 was blocked by a gain-of-function mutation in ced-9 but was not dependent on ced-3 function, suggesting that CED-4 translocation precedes