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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. |
| 盡管目前已經(jīng)知道遺傳多樣性受污染的影響(Bickham et al.,2000; Belfiore and Anderson, 2001 for a review),在某些方面這項(xiàng)研究還是新的。首先,我們的研究關(guān)注的是由于高脂肪含量而極端受到污染的物種的生物量積累水平,這反映了有機(jī)體受到的實(shí)際污染壓力(Collings et al., 1996)。它們的逐漸衰弱的生活史有助于檢測出本地污染物對(duì)細(xì)胞體和遺傳特性的影響,因?yàn)橛啄牦w與本地再生的及遺傳特性不同的淡水品種相比,進(jìn)入河中時(shí)攜帶很少的污染量和不同的遺傳學(xué)背景。在河中呆幾年時(shí)間后的生物量積累水平可以用來指示它們的健康狀況,因?yàn)槭軓?qiáng)烈污染的鰻魚去毒不明顯,狀態(tài)不好,可能不會(huì)成為成功的產(chǎn)卵魚(Feunteun, 2002)。其次,已經(jīng)證明幾個(gè)遺傳標(biāo)記可以用于區(qū)別選擇的影響,還有一些標(biāo)記可能是特意標(biāo)記(Belfiore and Anderson, 2001)。這個(gè)研究中,我們比較了用帶有酶學(xué)標(biāo)記(等位基因酶)的嚴(yán)格中立的遺傳標(biāo)記(微衛(wèi)星DNA)得到的品種,因?yàn)檫x擇中立性的假說多次被質(zhì)疑(Eanes, 1999)。得到生物測定(重量,條件,生長)相應(yīng)曲線的重要性也被強(qiáng)調(diào)為一種測定污染對(duì)有機(jī)體的影響的方法(Van Straalen and Timmermans, 2002)。最后,由于定義生物相關(guān)性群體很困難,對(duì)向鰻魚這樣高度游離的,具逐漸衰弱的生活史的有機(jī)體的研究仍然不具足夠的代表性。早期的研究用的是再生的分離群體,使得根據(jù)“遺傳侵蝕”假說比較直接得到的群體成為可能(Van Straalen and Timmermans, 2002)。這里,我們用兩種方法解釋了這個(gè)問題,一是估計(jì)污染對(duì)遺傳多樣性的影響(“遺傳侵蝕”假說),二是考慮個(gè)體遺傳多樣性應(yīng)對(duì)污染時(shí)的優(yōu)勢(“雜種優(yōu)勢”或者“超顯性”假說)。無論怎樣,由于鰻魚的逐漸衰弱的生活史和其喪失育性,我們的觀察得不出進(jìn)化結(jié)果的有力結(jié)論。 |

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