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马氏珠母贝(Pinctada martensii)2个不同地理种群遗传变异的EST-SSR分析
  • 期刊名称:海洋与湖沼
  • 时间:0
  • 页码:1059-1068
  • 语言:中文
  • 分类:Q953[生物学—动物学]
  • 作者机构:[1]热带生物资源教育部重点实验室海南大学海洋学院海南省热带水生生物技术重点实验室,海口570228
  • 相关基金:国家高技术研究发展计划(863计划)资助项目,2006AA10A409号;科技部农业科技成果转化资金项目,2006GB2E200236号:国家自然科学基金资助项目,40676075号、30460105号.
  • 相关项目:马氏珠母贝养殖群体对海南岛东部野生种群遗传多样性的影响
中文摘要:

应用17个EST-SSR位点分析表明,马氏珠母贝印度种群和三亚种群的平均FST值为0.486,两个种群的分化程度高;三亚种群的等位基因数为1—6,有效等位基因数为1.0—3.3;印度种群的等位基因数为2—7,有效等位基因数为1.1—3.3;三亚种群和印度种群的平均有效等位基因数分别是1.8和1.9;三亚种群和印度种群的等位基因丰度分别为3.16和3.39;印度种群无论是期望杂合度(HE)还是观察杂合度(HO)都高于三亚种群,印度种群的期望杂合度和观察杂合度分别是0.42和0.16;三亚种群的期望杂合度和观察杂合度分别是0.38和0.15;三亚种群与印度种群的Nei’s遗传距离为1.119。两个种群都保持了中等水平遗传多样性。由于两个种群高度的遗传分化和保持丰富的遗传多样性为开展两个种群间杂交及获得杂种优势奠定了基础。

英文摘要:

Two geographical populations of pearl oyster, Pinctada martensii, from India (IN) and Sanya (SY) were selected as key members to constitute a hybrid breeding system with heterosis. Analysis of 12% polyacrylamide gel elec- trophoresis (PAGE) on 17 EST-SSRs (microsatellites) indicated high differentiation between SY and IN (mean FST = 0.486) The total number of allele (a) and effective number of alleles (ne) were 1--6 and 1.0--3.3 for SY, and 2--7 and 1.1--3.3 for IN. The average effective number was 1.8 and 1.9, and the allele richness per locus (Rs) were identified as 3.16 and 3.39, respectively. Both expected heterozygosity (HE) and observed heterozygosity (Ho) of IN are higher than those of SY: 0.42 and 0.16 versus 0.38 and 0.15. The Fixation Indices (Fls) of SY was 0.67, and 0.68 for IN. The Nei's genetic distance between two populations is 1.119, suggesting that they were in a moderate level of genetic diversity. The traits of IN and SY populations are highly complementary, and expected to show heterosis in hybrid generations. Furthermore, comparative analysis in Hardy-Weinberg equilibrium (HWE) demonstrated significant genotypic disequilibrium of polymorphic sites in both populations: 10 out of 16 (62.5%, P〈0.001) for SY and 13 out of 17 (76.47%, P〈0.001) for IN. The EST-SSR sites with HWE disequilibrium appeared heterozygote deficiency, which caused possibly by null alleles.

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