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Although the impact of pollution on genetic variability has been assessed previously (Bickham et al.,2000; Belfiore and Anderson, 2001 for a review), this study is novel in several aspects. First, our study focused on the level of bioaccumulation in a species extremely prone to pollution due to its high fat content,reflecting the actual pollution stress in the organism(Collings et al., 1996). Its catadromous life historyenables the detection of local pollutant influences on somatic and genetic characteristics, as juveniles enter rivers with much less pollution load or differential genetic background than locally reproducing and genetically distinct freshwater species. Their level of bioaccumulation after a few years spent in the rivers can be considered as indicative of their fitness, because strongly polluted eels detoxify less efficiently, have a lower condition and might be less successful spawners (Feunteun, 2002). Secondly, it has been suggested that several genetic markers should be used to discriminate between the influence of selection and other factors that might be marker specific (Belfiore and Anderson, 2001). In this study we compared patterns from strictly neutral genetic markers (microsatellite DNA) with enzymatic markers (allozymes), for which the assump- tion of selective neutrality has often been challenged(Eanes, 1999). The significance of assessing biometric (weight, condition, growth) responses has also been underlined as a measure of pollutant impact on the organism(Van Straalen and Timmermans, 2002). Finally,the study of highly vagile organisms with a catadromous life-history like eel remains underrepresented,due to the difficulty of defining biologically relevant populations. Earlier studies used reproductively isolated populations, enabling straightforward population comparisons in the light of the “genetic erosion” hypothesis (Van Straalen and Timmermans, 2002). Here, we explain this issue in two ways, namely (1) by assessing the impact of pollutants on genetic variability (“Genetic Erosion” hypothesis) and (2) by considering individual genetic variability as an advantage to cope with pollution (“Heterosis” or “overdominance”hypothesis). Nevertheless, due to the catadromous lifehistory of eel and its failure to breed in captivity, no strong conclusions about evolutionary consequences can be drawn from our observations. |
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wypward(金币+2):谢谢参与 2010-09-20 20:51:18
ringzhu(金币+5, 翻译EPI+1): 2010-11-22 12:46:30
ringzhu(金币+5):辛苦了 这么一长段 不容易啊 楼主太小气了 才给5个 姐姐再给你5个 鼓励一下 哈哈~~~ 2010-11-22 12:47:07
wypward(金币+2):谢谢参与 2010-09-20 20:51:18
ringzhu(金币+5, 翻译EPI+1): 2010-11-22 12:46:30
ringzhu(金币+5):辛苦了 这么一长段 不容易啊 楼主太小气了 才给5个 姐姐再给你5个 鼓励一下 哈哈~~~ 2010-11-22 12:47:07
| 尽管目前已经知道遗传多样性受污染的影响（Bickham et al.,2000; Belfiore and Anderson, 2001 for a review），在某些方面这项研究还是新的。首先，我们的研究关注的是由于高脂肪含量而极端受到污染的物种的生物量积累水平，这反映了有机体受到的实际污染压力(Collings et al., 1996)。它们的逐渐衰弱的生活史有助于检测出本地污染物对细胞体和遗传特性的影响，因为幼年体与本地再生的及遗传特性不同的淡水品种相比，进入河中时携带很少的污染量和不同的遗传学背景。在河中呆几年时间后的生物量积累水平可以用来指示它们的健康状况，因为受强烈污染的鳗鱼去毒不明显，状态不好，可能不会成为成功的产卵鱼(Feunteun, 2002)。其次，已经证明几个遗传标记可以用于区别选择的影响，还有一些标记可能是特意标记(Belfiore and Anderson, 2001)。这个研究中，我们比较了用带有酶学标记（等位基因酶）的严格中立的遗传标记（微卫星DNA）得到的品种，因为选择中立性的假说多次被质疑(Eanes, 1999)。得到生物测定（重量，条件，生长）相应曲线的重要性也被强调为一种测定污染对有机体的影响的方法(Van Straalen and Timmermans, 2002)。最后，由于定义生物相关性群体很困难，对向鳗鱼这样高度游离的，具逐渐衰弱的生活史的有机体的研究仍然不具足够的代表性。早期的研究用的是再生的分离群体，使得根据“遗传侵蚀”假说比较直接得到的群体成为可能(Van Straalen and Timmermans, 2002)。这里，我们用两种方法解释了这个问题，一是估计污染对遗传多样性的影响（“遗传侵蚀”假说），二是考虑个体遗传多样性应对污染时的优势（“杂种优势”或者“超显性”假说）。无论怎样，由于鳗鱼的逐渐衰弱的生活史和其丧失育性，我们的观察得不出进化结果的有力结论。 |
2楼2010-09-19 19:04:53
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