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通过微卫星分子标记对来自安徽省4个草鱼养殖群体进行遗传分析。结果表明,7个微卫星位点均具有高度多态性(PIC=0.863～0.926),4个草鱼群体均显示出较高的遗传多样性(He=0.886 1～0.911 4)。AMOVA分析显示,大多数遗传变异存在于草鱼群体内(97.6%),群体间的遗传变异仅为2.4%。遗传分化和遗传距离分析显示,4个群体整体分化水平较低(Fst0.05),怀远和滁州群体遗传分化最小(Fst=0.013 7),遗传距离最近(Dn=0.269 8),池州和无为群体遗传分化最大(Fst=0.042 5),遗传距离最远(Dn=0.591 6)。系统进化树显示,怀远和滁州群体亲缘关系最近,与池州最远。此外,4个养殖场内部草鱼均存在近亲繁殖现象。建议4个养殖场及时更新亲本,增加繁殖亲本的数量,避免近交衰退带来的风险。 相似文献
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应用基于分子标记的主成分分析法、贝叶斯遗传聚类法和遗传重排技术对鲤4个人工选育群体(兴国红鲤、荷包红鲤、玻璃红鲤和建鲤)和2个长江干流天然群体(湖北监利和江苏扬州)的10个微卫星标记结果进行分析,以有效检测人工选育群体间以及选育群体与天然群体间的遗传差异。主成分分析显示,人工选育群体与天然群体存在一定程度的遗传分化,荷包红鲤与天然群体的遗传差异最大,其主成分1(PC1)和主成分2(PC2)解释了总遗传变异的48.23%;在贝叶斯遗传聚类分析中,6个群体的最佳聚类数值为4,即兴国红鲤与2个天然群体聚为一类,玻璃红鲤、荷包红鲤和建鲤3个群体分别单独聚为一类;贝叶斯遗传重排分析显示,6个群体的遗传自排率较高,为81%～100%,玻璃红鲤和荷包红鲤的遗传自排率最高,均为100%。研究结果综合表明:4个人工选育群体与天然群体间存在较明显的遗传差异,而且天然群体已受到人工选育群体的遗传影响;这3种方法能很好地检测鲤人工选育群体间、以及选育群体与天然群体间的遗传差异。 相似文献
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利用20对微卫星标记埘长鳍鲤、锦鲤和龙凤鲤3个鲤鱼群体的遗传多样性和遗传结构进行分析.结果表明:3个群体在20个位点上分别检测到108、164、154个等位基因,各群体等位基因数2～16个不等,平均有效等位基因数分别为4.496、5.695和5.606.3个群体平均期望杂合度分别为0.769、0.806、0.801,多态信息含量分别为0.703、0.761和0.757,遗传多样性指数分别为0.764、0.803和0.799,群体间遗传分化系数为0.071.结果说明3个群体遗传多样性较为丰富. 相似文献
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利用微卫星标记分析6个鲤鱼群体的遗传差异 总被引：2，自引：0，他引：2
为了评估和合理利用鲤种质资源,选出13个微卫星位点对框镜鲤、黑龙江鲤、荷包红鲤、兴国红鲤、黄河鲤和建鲤进行遗传多样性分析。结果显示:13个微卫星位点在6个鲤鱼群体中共检测出142个等位基因,所检测到的等位基因片段长度在116～280bp。各鲤鱼群体的平均观察杂合度(Ho)、期望杂合度(He)分别在0.564～0.705和0.611～0.776;13个位点在6个鲤鱼群体中平均多态信息含量(PIC)在0.573～0.749。固定系数(FIS)分析表明,只有建鲤群体表现为杂合子过剩(平均FIS<0),其他5个鲤鱼群体表现为杂合子缺乏(平均FIS>0)。试验结果表明,这6个鲤鱼群体多态信息含量丰富,遗传多样性水平较高,具有较大的选育潜力。群体间的遗传距离和聚类分析显示,框镜鲤与兴国红鲤亲缘关系最远,黄河鲤与建鲤的亲缘关系最近。 相似文献
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利用微卫星标记分析云南省6个东方蜜蜂(Apis cerena)群体遗传多样性及遗传分化 总被引：2，自引：0，他引：2
利用21对微卫星标记对来自于腾冲、无量山、迪庆、武定、泸水、西双版纳6个云南东方蜜蜂Apis cerana群体进行遗传多样性及遗传分化分析.通过计算多态信息含量、平均杂合度、等位基因数、遗传距离、基因流、F-统计量等参数,评估各东方蜜蜂群体遗传多样性和各群体间遗传分化.各座位的等位基因数为4(AP313)至18(AT003).除迪庆群体外,其余群体均显示较高水平的期望杂合度,其中,武定群体最高,为0.696;迪庆群体最低,为0.367.各东方蜜蜂群体间存在极显著的遗传分化,平均分化系数Fst为0.264.云南6个东方蜜蜂群体的遗传分化显著,除迪庆群体外,其余5个群体遗传多样性较高;分析遗传分化与地理距离的关系发现,云南6个东方蜜蜂群体间的遗传分化与地理距离不存在显著相关. 相似文献
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为研究新疆伊犁地区喀什河谷流域密叶杨遗传多样性及群体遗传结构与空间地理位置上、中、下游变化的关系,选用26对微卫星标记对220个个体的遗传多样性进行了分析,共检测到163个等位基因,平均等位基因数(Na)为6.629;多态性位点百分率(PPL)为100%,期望杂合度(He)在上、中、下游3个群体中都处于较高水平,分别为0.548、0.567和0.591;分子方差分析(AMOVA)的结果表明,7%的遗传分化来自种群间,遗传变异主要集中在群体内不同个体之间;基因分化系数(Gst)为0.038,表明群体分化处于较低水平,而检测到群体间的基因流(Nm)则为12.818,处于较高水平。表明密叶杨种群的遗传多样性在空间地理位置上未产生分化,遗传多样性水平较高。并提出了密叶杨种群保护策略。 相似文献
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秦溱 《湖南农业大学学报(自然科学版)》2014,40(3)
利用AFLP分子标记方法对4个群体(福建连江野生、连江养殖、长乐养殖、广西野生)的泥东风螺进行遗传多样性分析。结果:用11对引物共扩增出908条有效片段,其中684条(75.33%)为多态性片段,224条片段(24.67%)为4个群体所共有;遗传多样性指数分析显示,4个群体的有效等位基因数、平均等位基因数、Shannon’s多样性指数和平均杂合度依次为1.500 6、1.974 0、0.464 7、0.303 4,Nei’s遗传距离为0.128 4~0.180 6,遗传相似系数为0.834 8~0.879 5,表明4个泥东风螺群体具有较为丰富的遗传多样性,且群体间具有较高的遗传相似性;分子方差分析(AMOVA)结果显示,4个群体中83.49%的变异来源于群体内,14.65%的变异来源于地区间,而群体间的遗传变异仅为1.86%,且4个群体间的遗传分化(GST)为0.195 4,基因流(NM)为2.058 6,说明群体间的基因交流水平较低;UPGMA聚类分析和主坐标(PCA)分析结果表明,长乐养殖群体和广西野生群体遗传距离最近,而连江野生群体与其他3个群体的遗传距离最远。 相似文献
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为探究江浙地区不同罗氏沼虾(Macrobrachium rosenbergii)群体的遗传多样性和遗传结构,利用16个微卫星标记对潮丰(CF)、蓝天(LT)、源泉A(YQA)、源泉B(YQB)、嘉丰(JF)、南太湖(NTH)等6个江浙地区养殖群体和1个泰国正大(ZD)引进群体进行遗传变异分析.结果显示,16个微卫星位点均为高度多态位点;7个群体均为较高的遗传多样性,期望杂合度(He)和多态信息含量(PIC)均大于0.7,遗传多样性大小排序为ZD>YQA>YQB>JF>LT>NTH>CF;遗传分化指数(Fst)分析结果显示,泰国正大与江浙地区各群体间存在中等程度的遗传分化,Fst介于0.10145～0.12348之间;江浙地区群体除NTH与CF群体间为中等程度遗传分化(Fst=0.05098)外,其余群体间的遗传分化程度较低,Fst介于0.01571～0.04099之间.AMOVA分析结果显示,遗传变异主要发生在个体内和群体内个体间,群体间遗传变异仅占2.10％.依据Nei's遗传距离构建的非加权组平均法(UPGMA)系统进化树显示,泰国正大群体独占一支,江浙地区6个群体聚为另一支.Structure分析结果显示,所有样本被划分为2个理论群,江浙地区6个群体为一个集群,泰国正大群体为一个集群.该研究不但揭示了江浙地区罗氏沼虾养殖群体的遗传多样性现状,而且也为罗氏沼虾种质资源的保护、利用以及优良品种的选育提供了参考信息. 相似文献
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安徽淮河水系黄鳝群体遗传多样性及其遗传结构 总被引：1，自引：1，他引：1
利用线粒体Cyt b基因全序列(1138 bp)对安徽淮河水系黄鳝6个地理群体(阜南Fn、颍上Ys、平圩Pw、怀远Hy、凤阳Fy、明光Mg)165个样品进行遗传多样性和遗传结构分析。共检测到变异位点74个、单倍型25个,平均A+T含量(54.8%)显著大于G+C(45.2%)含量。平均单倍型多样性和平均核苷酸多样性分别为0.787、0.01882。各群体的遗传分化指数FST为0.01933~0.81352、基因流Nm为0.11461~26.36650,分子方差分析(AMOVA)显示44.1%的变异来自群体间,表明淮河水系黄鳝地理群体间存在较高程度的遗传分化。单倍型系统进化树和进化网络图揭示安徽淮河黄鳝6个群体的个体组成2个遗传差异明显的谱系。错配分布和中性检验结果表明安徽淮河黄鳝群体历史上较为稳定,无明显群体扩张。 相似文献
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Crow JF 《Science (New York, N.Y.)》1987,236(4807):1475-1476
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Integration of molecular genetic technology with quantitative genetic technology for maximizing the speed of genetic improvement 总被引：1，自引：0，他引：1 
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下载免费PDF全文 Jack C.M. DEKKERS 《华南农业大学学报》2005,26(Z1)
To date,most genetic progress for quantita-tive traits in livestock has been made by selec-tion on phenotype or on estimates of breedingvalues(BBV)derived from phenotype,withoutknowledge of the number of genes that affect thetrait or the effects of each gene.In this quantita-tive genetic approach to genetic improvement,the genetic architecture of traits of interest hasessentially been treated as a‘black box’.De-spite this,the substantial rates of genetic im-provement that have been and continue to be a-chie... 相似文献
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福建若干荔枝古树资源的RAPD分析 总被引：4，自引：1，他引：4
利用随机扩增多态性DNA(RAPD)技术,从104个十聚体随机引物筛选出13个引物对福建荔枝著名的古树以及相关品种等12份材料的基因组DNA进行扩增,共得到78条扩增谱带,其中2条为共同带,多态性程度达97.44%,平均每条引物扩增的谱带数目为6条.采用遗传标记计算遗传资源相似性系数,进行聚类分析,并构建树状分析图.结果表明:现在栽培的陈紫品种与宋家香的亲缘很近,可能来源于宋家香;而元红与西禅寺“宋荔”亲缘关系较远.应用RAPD技术为荔枝古树遗传资源的鉴定和分类提供了新的途径. 相似文献
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巴什拜羊群体遗传多样性与遗传分化的研究 总被引：1，自引：0，他引：1
利用10个微卫星标记对新疆巴什拜羊4个品系(红毛、白毛、黑毛和瘦肉型新品系)189个个体进行检测,分析群体遗传多样性和群体间的遗传分化、系统发育关系。结果表明:在巴什拜羊10个微卫星座位中共检测到110个等位基因,平均每个座位等位基因数为11个;4个群体10个微卫星标记的平均多态信息含量为0.791 4,平均杂合度为0.814 9,说明巴什拜羊4个群体均具有丰富的遗传多样性;4个绵羊群体的总近交系数为-0.178 2,群体内近交系数为-0.211 2,群体间基因分化系数为0.023 7,说明4个绵羊群体间2.37%的遗传变异来自群体间,而97.63%的遗传变异是由各群体内个体间的差异引起的;基因流(Nm)平均值为8.916 7。聚类分析发现,红毛品系与黑毛品系亲缘关系较近,之后与白毛品系相聚,最后与瘦肉型新品系聚在一起,聚类结果与品系育成史基本一致。 相似文献
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Our vanishing genetic resources 总被引：2，自引：0，他引：2
Harlan JR 《Science (New York, N.Y.)》1975,188(4188):617-621
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LSD and genetic damage 总被引：3，自引：0，他引：3
Of nine studies in vitro, six have indicated some degree of induced chromosomal breakage after exposure to LSD; three failed to confirm these results. The damage, when found, was generally of the chromatid type, arising during or after DNA synthesis. This damage, with one exception, was the result of concentrations of drug and durations of exposure which could not be achieved in humans with reasonable dosages. There did not appear to be a dose-response relation. The magnitude of damage, when found, was in the range encompassing the effects of many commonly used substances. The absence in vitro of excretory and detoxifying systems present in vivo, as well as several negative reports, cast doubt on the relevance of in vitro results. In 21 chromosomal studies in vivo, 310 subjects were examined. Of these, 126 were treated with pure LSD; the other 184 were exposed to illicit, "alleged" LSD. A maximum of only 18 of 126 (14.29 percent) of the subjects in the group exposed to pure LSD showed higher frequency of chromosome aberration than the controls. In contrast, a maximum of 90 of 184 (48.91 percent) of the subjects taking illicit LSD showed an increase in frequency of aberrations. Of all the subjects reported to have chromosome damage, only 18 of the 108 (16.67 percent) were exposed to pure LSD. The frequency of individuals with chromosomal damage reported among illicit drug users was more than triple that associated with the use of pharmacologically pure LSD. We conclude that chromosome damage, when found, was related to the effects of drug abuse in general and not, as initially reported, to LSD alone. We believe that pure LSD ingested in moderate dosages does not produce chromosome damage detectable by available methods. No significant work on carcinogenic potential of LSD has been reported so far. No cause-and-effect relation and no increase in the incidence of neoplasia among LSD users have been demonstrated. Case reports (three in 4.0 years) of leukemia and other neoplasia in this population are rare. The results of early chromosome studies suggested that true genetic damage might be a consequence of LSD exposure. The comprehensive evidence from studies on drosophila indicates no mutagenic effect from 0.28 to 500 microg of LSD per milliliter and a definite mutagenic effect from 2,000 to 10,000 microg/ml; this is consistent with a threshold response or a sigmoid dose-effect relation. We believe that LSD is, in fact, a weak mutagen, effective only in extremely high doses; it is unlikely to be mutagenic in any concentration used by human subjects. Circular dichroism experiments suggested that the specific mechanism of action of LSD on DNA may be a direct interaction resulting in conformational changes in the DNA helix. These changes are unlikely to result in a decrease of internal stability sufficient to cause breakage of chromosomes, but they may be the physical basis of the weak mutagenicity. Early chromosomal studies implicated LSD as a potential cause of congenital malformations, fetal wastage, and germinal chromosome damage. First reports of a teratogenic effect in hamsters and rats have not been confirmed. A review of 15 rodent studies indicated a wide range of individual, strain, and species susceptibility to the effects of LSD. The applicability of such investigations to man is doubtful. In a study of human pregnancies, those exposed to illicit LSD had an elevated rate of spontaneous abortions. There is no reported instance of a malformed child born to a woman who ingested pure LSD; there are six cases of malformation associated with exposure to illicit LSD, four of which have similar limb defects. Given, however, the high frequency of unexplained "spontaneous" birth defects, the rare occurrence of malformed infants born to women who used illicit LSD may be coincidental. While there is no evidence that pure LSD is teratogenic in man, the use of any drug during pregnancy requires that its potential benefits significantly outweigh its potential hazards. From our own work and from a review of the literature, we believe that pure LSD ingested in moderate doses does not damage chromosomes in vivo, does not cause detectable genetic damage, and is not a teratogen or a carcinogen in man. Within these bounds, therefore, we suggest that, other than during pregnancy, there is no present contraindication to the continued controlled experimental use of pure LSD. Note added in proof: A brief review has been brought to our attention. Although based on a sample of only 15 studies the author reached conclusions similar to our own (92). 相似文献
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