中国小麦白粉病主要流行区病原菌群体遗传结构研究
|
摘要
由Blumeria graminis f. sp. tritici引起的小麦白粉病，是一种世界性真菌病害，也是我国小麦生产上发病面积最大、危害损失最重的常发性病害。其病原物小种多、变异快、侵染时期长、气流传播、适应范围广，群体结构较为复杂。为了对病菌毒性基因变化动态及抗病基因的抗性丧失作出早期预测，从分子水平揭示病原菌群体遗传变异和区间传播规律，为制定更为有效的病害控制策略提供基础，本研究利用一套鉴别品系，分析病原菌群体对现有已知抗病基因的毒性频率，明确其毒性结构，利用中性遗传标记探索不同流行区病原菌群体分子遗传结构，并结合高空气流的轨迹分析，寻找病菌孢子远程传播的佐证。
小麦白粉菌标样于2010年和2011年采集于我国西南（贵州、重庆、四川）、西北（青海、甘肃、陕西）、中部（湖北、安徽、河南）和华北（河北、北京）4个流行区11个省市，经两次单孢子堆分离纯化，共获得674份试验菌株。利用34个已知抗白粉病基因品种（系）对其中418份菌株进行苗期毒性测定，采用AOX、PKA、PPA三个基因位点的SNPs标记对674份菌株进行分子遗传结构的研究，并应用Hysplit_4软件对两年病菌孢子春季迁移的气流轨迹进行分析。现将试验获得的结果总结如下：
（1）明确了2010年和2011年我国小麦白粉病主要流行区病原菌群体的毒性结构。
同一年度不同省市群体间毒性结构基本相似，个别毒性基因频率存在一定的差异。相同省市群体年度间毒性水平略有上升或下降。两年中供试群体对抗性基因Pm1a、Pm3a、Pm3b、Pm3c、Pm3e、Pm5a、Pm6、Pm7、Pm8、Pm17、Pm19、Pm25和Pm34的毒性频率整体上均在55%-100%之间，说明与之对应的毒性基因分布较广，抗性基因抗性较差，在生产上已不能作为抗源使用。含Pm12、Pm13、Pm16和Pm21等基因的品种在两年中均表现出较好的抗性，可作为当前我国防治小麦白粉病的有效抗源加以利用。
（2）从毒性上揭示了我国小麦白粉菌群体具有较高的遗传变异和较低的遗传分化。
毒性分析结果显示，每个菌株对9-29个Pm基因表现出致病性，菌株毒谱较宽。两年测试群体Nei基因多样性指数H分别是0.274和0.268，Shannon信息指数I分别为0.408和0.399，多态性位点百分率P%分别为94.12%和82.35%，表明我国小麦白粉菌群体具有较高的毒性多样性。PopGen软件遗传分化分析两年结果均显示，低于10%的变异存在于群体间，超过90%的变异来自于群体内。AMOVA分析表明，区组间、区组内群体间及群体内都存在着一定程度的遗传分化，但88%以上的遗传变异主要来源于群体内。PCA主成分分析显示，菌株群体间交叉并存，各群体内菌株分布既集中又分散，再次说明病原菌群体间低水平分化而群体内高水平变异。
（3）从分子水平上揭示了我国小麦白粉菌群体具有较高的遗传多样性。
三个基因片段的多位点序列分析结果显示，拼接序列全长2316bp，排除gaps和缺失位点45个，共发现19个变异位点，其中单一信息位点7个，简约信息位点12个。两年共检测到45种单倍型，其中单倍型H1和H2分布范围最广，占整个样本的44.8%。稀有单倍型共计15种，占整个样本的3.26%。群体单倍型多样度Hd值两年分别为0.8592和0.9027，表明我国小麦白粉菌群体具有较高水平的遗传多样性。
（4）探索了我国小麦白粉菌群体分子遗传结构。
单倍型的NJ系统发育树和网络关系进化图显示，单倍型的分布没有呈现出明显的地理族群，各地理群体间遗传分化程度相对比较低。回归分析表明群体分子遗传变异存在一定程度的地理分化。AMOVA分析显示，区组间、区组内群体间及群体内都存在着一定程度的遗传分化，但两年中分别有92.44%和73.01%的遗传变异主要来源于群体内，揭示地理隔离不是造成我国小麦白粉菌群体间遗传分化的主导因素。核苷酸错配分布呈现多峰模式，且中性检验Tajima’s D值(-0.84732)与Fu’s Fs值(-40.768）均不显著（P>0.05），说明我国分布的小麦白粉菌群体在较近的历史时期内没有经历过群体扩张事件，群体大小保持相对稳定。
（5）证实了病原菌群体间存在病菌的重组和迁移。
DnaSP分析检测到最小重组事件数为5，表明群体中存在有性重组。群体间基因流两两比较分析显示，大多数Nm值均高于4，甚至远大于4，表明基因交流十分频繁。高频次单倍型的广泛分布，同样说明不同地区间菌源有迁移；而稀有单倍型的发现，表明群体内存在独立进化。利用Hysplit_4软件对两年春季菌源迁移的气流轨迹进行分析，结果均表明，西南菌源主要影响西南、西北、中部和华北麦区，西北菌源主要影响西北、中部、华北和四川麦区，中部菌源主要影响中部和华北麦区，华北菌源主要影响华北和东北麦区。此结果与基因流的检测值互为印证，再次证实我国小麦白粉病主要流行区病原菌群体既存在远距离传播又具有本地进化，也为小麦白粉菌能够在我国大部分地区完成其周年侵染循环这一理论推断提供了分子和高空气流的佐证。
（6）明确了我国小麦白粉菌群体遗传多样性中心。
毒性多样性和单倍型多样度分析表明，我国西南和西北群体其遗传多样性总体评价要比中部和华北群体高，特别是重庆、四川和甘肃群体，其单倍型数目多、类型广，且分别与其他省市群体存在高强度的基因流。春季菌源迁移轨迹分析同样表明，西南和西北菌源可直接或间接影响到全国其他流行区。据此，我们推断，西南麦区和甘肃麦区为我国小麦白粉菌遗传多样性中心。
Wheat powdery mildew, caused by obligate parasitic fungus Blumeria graminis f. sp. tritici (Bgt),is a worldwide wheat disease. In China, this disease is recurrent with the largest area of incidence andthe heavy losses. The pathogen has high evolutionary potential as a result of a mixed reproductionsystem, a large population size, a wide adaptation and wind-aided dispersal mode. Analysis on the Bgtvirulence and molecular genetic structure from major epidemic zones of China, combining with airparcel trajectory to seek the evidence of pathogen long-distance dispersal, will be important to themonitoring and early forecasting of the virulence dynamics of the pathogen population and the ‘loss’ ofresistance in host, to reveal pathogen population genetic variation and the dissemination betweendifferent regions from the molecular level, and can be used to guide the disease management strategies.
In this study, a collection of674single-colony wheat powdery mildew isolates were recoveredfrom samples collected in2010and2011, covering the regions of the southwest (Guizhou, Chongqing,Sichuan), the northwest (Qinghai, Gansu, Shaanxi), the central (Hubei, Anhui, Henan) and North China(Hebei, Beijing). To gain more precise information about pathogen population structure, we pursued acombined pathological and genetic approach. Additionally, air parcel trajectory of the spore transportsof the pathogen were investigated by using Hysplit_4based on meteorological data in spring. The mainresults obtained are as follows:
(1) Determined Bgt virulence structure from major epidemic zones of China in the two years.
A total of418isolates were inoculated onto34differential wheat lines of powdery mildew. Theresults showed the virulence frequencies were nearly the same among different provinces in each yearexcept a few genes, and small changes existed between years. Over55%of the isolates were virulent toPm3a, Pm3b, Pm3c, Pm3e, Pm5a, Pm6, Pm7, Pm8, Pm17, Pm19, Pm25, and Pm34in both years. Thevirulence frequency was low to Pm12, Pm13, Pm16, and Pm21, indicating effective resistant resources.
(2) Revealed a high genetic variation within populations but a lower genetic differentiation amongpopulations based on virulence factors.
The estimation of virulence complexity showed each isolate was virulent to9-29Pm genes. Nei’sgenetic diversity index, Shannon’s information index, and polymorphism loci percentage were0.274,0.408,94.12%in2010, and0.268,0.399,82.35%in2011, respectively, revealing high virulencediversity. Genetic differentiation analysis from PopGen showed less than10%of the variation existedamong populations and more than90%of the variation within populations in both years. Analysis ofmolecular variance (AMOVA) and principal coordinate graph (PCA) revealed similar results, indicatinga high genetic variation within populations but a lower genetic differentiation among populations.
(3) Revealed a high level of genetic diversity from the molecular level.
A total of2316nucleotides from three house-keeping gene regions, Alternative oxidase (AOX),Protein kinase A (PKA) and Protein phosphatase type2A (PPA), for674isolates were sequenced.19variable characters were detected from multilocus sequences, comprised of7singleton variable sitesand12parsimony informative sites.45haplotypes (H1-H45) were inferred in total, with H1and H2 comprising over44.8%of the populations, and15rare haplotypes consisting of3.26%of thepopulations. The haplotype diversity for2010population was0.8592and0.9027for2011, indicating ahigh level of genetic diversity.
(4) Explored molecular genetic structure of the pathogen population.
Neighbor-joining phylogenetic tree and minimum spanning network based on haplotypes did notshow obvious geographical subdivision. Regression analysis indicated there was a certain degree ofgeographic differentiation among populations. AMOVA analysis revealed92.44%of the total variationwithin populations in2010and73.01%of that in2011, suggesting distance isolation was not the mainfactor causing Bgt population genetic differentiation and there was difference between years. Mismatchdistributions of multilocus sequences presented a bimodal fashion, and Tajima’s D value (-0.84732) andFu’s Fs value (-40.768) were not significant (P>0.05), implying that there might not be a populationexpansion in recent time and mildew populations was at demographic equilibrium.
(5) Confirmed genetic recombination and pathogen long-distance migration.
5minimum recombination events were detected from variable sites, proving the existence ofsexual recombination. Most of pairwise Nm values between populations were higher than4, suggestinga frequent gene exchange among populations. The findings of shared dominant haplotypes confirmedthis. The distributions of rare haplotypes revealed local evolution. Trajectory analysis in two yearssuggested that the inoculum sources in Southwestern China mainly affect the disease epidemics inSouthwestern, Northwestern, Central, and Northern China in spring. The sources in Northwestern Chinaaffected mainly on Northwestern, Central, Northern China, and Sichuan. The sources in Central Chinamainly cover Central and Northern China. The pathogen from Northern China could be dispersed withinthe region and to Northeastern China. All of these evidences support the existence of the frequentlong-distance migration of Bgt populations among different regions in China and independent evolutionwithin the regions.
(6) Clarified the center of Bgt genetic diversity.
The overall evaluation of virulence and genetic data showed a higher diversity in Southwestern andNorthwestern China than that in Central and Northern China, especially in Chongqing, Sichuan, andGansu populations. Trajectory analysis of spring spore transports indicated that the inoculum sources inSouthwestern and Northwestern China can impact the disease epidemics in other regions in Chinadirectly or indirectly. In view of this, we infer that Southwestern China and Gansu are the center of Bgtgenetic diversity, and speculate they may be the origin of Bgt in China.
小麦白粉菌标样于2010年和2011年采集于我国西南（贵州、重庆、四川）、西北（青海、甘肃、陕西）、中部（湖北、安徽、河南）和华北（河北、北京）4个流行区11个省市，经两次单孢子堆分离纯化，共获得674份试验菌株。利用34个已知抗白粉病基因品种（系）对其中418份菌株进行苗期毒性测定，采用AOX、PKA、PPA三个基因位点的SNPs标记对674份菌株进行分子遗传结构的研究，并应用Hysplit_4软件对两年病菌孢子春季迁移的气流轨迹进行分析。现将试验获得的结果总结如下：
（1）明确了2010年和2011年我国小麦白粉病主要流行区病原菌群体的毒性结构。
同一年度不同省市群体间毒性结构基本相似，个别毒性基因频率存在一定的差异。相同省市群体年度间毒性水平略有上升或下降。两年中供试群体对抗性基因Pm1a、Pm3a、Pm3b、Pm3c、Pm3e、Pm5a、Pm6、Pm7、Pm8、Pm17、Pm19、Pm25和Pm34的毒性频率整体上均在55%-100%之间，说明与之对应的毒性基因分布较广，抗性基因抗性较差，在生产上已不能作为抗源使用。含Pm12、Pm13、Pm16和Pm21等基因的品种在两年中均表现出较好的抗性，可作为当前我国防治小麦白粉病的有效抗源加以利用。
（2）从毒性上揭示了我国小麦白粉菌群体具有较高的遗传变异和较低的遗传分化。
毒性分析结果显示，每个菌株对9-29个Pm基因表现出致病性，菌株毒谱较宽。两年测试群体Nei基因多样性指数H分别是0.274和0.268，Shannon信息指数I分别为0.408和0.399，多态性位点百分率P%分别为94.12%和82.35%，表明我国小麦白粉菌群体具有较高的毒性多样性。PopGen软件遗传分化分析两年结果均显示，低于10%的变异存在于群体间，超过90%的变异来自于群体内。AMOVA分析表明，区组间、区组内群体间及群体内都存在着一定程度的遗传分化，但88%以上的遗传变异主要来源于群体内。PCA主成分分析显示，菌株群体间交叉并存，各群体内菌株分布既集中又分散，再次说明病原菌群体间低水平分化而群体内高水平变异。
（3）从分子水平上揭示了我国小麦白粉菌群体具有较高的遗传多样性。
三个基因片段的多位点序列分析结果显示，拼接序列全长2316bp，排除gaps和缺失位点45个，共发现19个变异位点，其中单一信息位点7个，简约信息位点12个。两年共检测到45种单倍型，其中单倍型H1和H2分布范围最广，占整个样本的44.8%。稀有单倍型共计15种，占整个样本的3.26%。群体单倍型多样度Hd值两年分别为0.8592和0.9027，表明我国小麦白粉菌群体具有较高水平的遗传多样性。
（4）探索了我国小麦白粉菌群体分子遗传结构。
单倍型的NJ系统发育树和网络关系进化图显示，单倍型的分布没有呈现出明显的地理族群，各地理群体间遗传分化程度相对比较低。回归分析表明群体分子遗传变异存在一定程度的地理分化。AMOVA分析显示，区组间、区组内群体间及群体内都存在着一定程度的遗传分化，但两年中分别有92.44%和73.01%的遗传变异主要来源于群体内，揭示地理隔离不是造成我国小麦白粉菌群体间遗传分化的主导因素。核苷酸错配分布呈现多峰模式，且中性检验Tajima’s D值(-0.84732)与Fu’s Fs值(-40.768）均不显著（P>0.05），说明我国分布的小麦白粉菌群体在较近的历史时期内没有经历过群体扩张事件，群体大小保持相对稳定。
（5）证实了病原菌群体间存在病菌的重组和迁移。
DnaSP分析检测到最小重组事件数为5，表明群体中存在有性重组。群体间基因流两两比较分析显示，大多数Nm值均高于4，甚至远大于4，表明基因交流十分频繁。高频次单倍型的广泛分布，同样说明不同地区间菌源有迁移；而稀有单倍型的发现，表明群体内存在独立进化。利用Hysplit_4软件对两年春季菌源迁移的气流轨迹进行分析，结果均表明，西南菌源主要影响西南、西北、中部和华北麦区，西北菌源主要影响西北、中部、华北和四川麦区，中部菌源主要影响中部和华北麦区，华北菌源主要影响华北和东北麦区。此结果与基因流的检测值互为印证，再次证实我国小麦白粉病主要流行区病原菌群体既存在远距离传播又具有本地进化，也为小麦白粉菌能够在我国大部分地区完成其周年侵染循环这一理论推断提供了分子和高空气流的佐证。
（6）明确了我国小麦白粉菌群体遗传多样性中心。
毒性多样性和单倍型多样度分析表明，我国西南和西北群体其遗传多样性总体评价要比中部和华北群体高，特别是重庆、四川和甘肃群体，其单倍型数目多、类型广，且分别与其他省市群体存在高强度的基因流。春季菌源迁移轨迹分析同样表明，西南和西北菌源可直接或间接影响到全国其他流行区。据此，我们推断，西南麦区和甘肃麦区为我国小麦白粉菌遗传多样性中心。
Wheat powdery mildew, caused by obligate parasitic fungus Blumeria graminis f. sp. tritici (Bgt),is a worldwide wheat disease. In China, this disease is recurrent with the largest area of incidence andthe heavy losses. The pathogen has high evolutionary potential as a result of a mixed reproductionsystem, a large population size, a wide adaptation and wind-aided dispersal mode. Analysis on the Bgtvirulence and molecular genetic structure from major epidemic zones of China, combining with airparcel trajectory to seek the evidence of pathogen long-distance dispersal, will be important to themonitoring and early forecasting of the virulence dynamics of the pathogen population and the ‘loss’ ofresistance in host, to reveal pathogen population genetic variation and the dissemination betweendifferent regions from the molecular level, and can be used to guide the disease management strategies.
In this study, a collection of674single-colony wheat powdery mildew isolates were recoveredfrom samples collected in2010and2011, covering the regions of the southwest (Guizhou, Chongqing,Sichuan), the northwest (Qinghai, Gansu, Shaanxi), the central (Hubei, Anhui, Henan) and North China(Hebei, Beijing). To gain more precise information about pathogen population structure, we pursued acombined pathological and genetic approach. Additionally, air parcel trajectory of the spore transportsof the pathogen were investigated by using Hysplit_4based on meteorological data in spring. The mainresults obtained are as follows:
(1) Determined Bgt virulence structure from major epidemic zones of China in the two years.
A total of418isolates were inoculated onto34differential wheat lines of powdery mildew. Theresults showed the virulence frequencies were nearly the same among different provinces in each yearexcept a few genes, and small changes existed between years. Over55%of the isolates were virulent toPm3a, Pm3b, Pm3c, Pm3e, Pm5a, Pm6, Pm7, Pm8, Pm17, Pm19, Pm25, and Pm34in both years. Thevirulence frequency was low to Pm12, Pm13, Pm16, and Pm21, indicating effective resistant resources.
(2) Revealed a high genetic variation within populations but a lower genetic differentiation amongpopulations based on virulence factors.
The estimation of virulence complexity showed each isolate was virulent to9-29Pm genes. Nei’sgenetic diversity index, Shannon’s information index, and polymorphism loci percentage were0.274,0.408,94.12%in2010, and0.268,0.399,82.35%in2011, respectively, revealing high virulencediversity. Genetic differentiation analysis from PopGen showed less than10%of the variation existedamong populations and more than90%of the variation within populations in both years. Analysis ofmolecular variance (AMOVA) and principal coordinate graph (PCA) revealed similar results, indicatinga high genetic variation within populations but a lower genetic differentiation among populations.
(3) Revealed a high level of genetic diversity from the molecular level.
A total of2316nucleotides from three house-keeping gene regions, Alternative oxidase (AOX),Protein kinase A (PKA) and Protein phosphatase type2A (PPA), for674isolates were sequenced.19variable characters were detected from multilocus sequences, comprised of7singleton variable sitesand12parsimony informative sites.45haplotypes (H1-H45) were inferred in total, with H1and H2 comprising over44.8%of the populations, and15rare haplotypes consisting of3.26%of thepopulations. The haplotype diversity for2010population was0.8592and0.9027for2011, indicating ahigh level of genetic diversity.
(4) Explored molecular genetic structure of the pathogen population.
Neighbor-joining phylogenetic tree and minimum spanning network based on haplotypes did notshow obvious geographical subdivision. Regression analysis indicated there was a certain degree ofgeographic differentiation among populations. AMOVA analysis revealed92.44%of the total variationwithin populations in2010and73.01%of that in2011, suggesting distance isolation was not the mainfactor causing Bgt population genetic differentiation and there was difference between years. Mismatchdistributions of multilocus sequences presented a bimodal fashion, and Tajima’s D value (-0.84732) andFu’s Fs value (-40.768) were not significant (P>0.05), implying that there might not be a populationexpansion in recent time and mildew populations was at demographic equilibrium.
(5) Confirmed genetic recombination and pathogen long-distance migration.
5minimum recombination events were detected from variable sites, proving the existence ofsexual recombination. Most of pairwise Nm values between populations were higher than4, suggestinga frequent gene exchange among populations. The findings of shared dominant haplotypes confirmedthis. The distributions of rare haplotypes revealed local evolution. Trajectory analysis in two yearssuggested that the inoculum sources in Southwestern China mainly affect the disease epidemics inSouthwestern, Northwestern, Central, and Northern China in spring. The sources in Northwestern Chinaaffected mainly on Northwestern, Central, Northern China, and Sichuan. The sources in Central Chinamainly cover Central and Northern China. The pathogen from Northern China could be dispersed withinthe region and to Northeastern China. All of these evidences support the existence of the frequentlong-distance migration of Bgt populations among different regions in China and independent evolutionwithin the regions.
(6) Clarified the center of Bgt genetic diversity.
The overall evaluation of virulence and genetic data showed a higher diversity in Southwestern andNorthwestern China than that in Central and Northern China, especially in Chongqing, Sichuan, andGansu populations. Trajectory analysis of spring spore transports indicated that the inoculum sources inSouthwestern and Northwestern China can impact the disease epidemics in other regions in Chinadirectly or indirectly. In view of this, we infer that Southwestern China and Gansu are the center of Bgtgenetic diversity, and speculate they may be the origin of Bgt in China.
引文
1.曹乃倩,刘桂茹,杨学举.小麦抗白粉病基因定位及分子标记辅助育种综述.中国农学通报,2007,23(7):482-486.
2.曹学仁,赵文娟,周益林,等.2007年我国部分麦区小麦白粉菌对三唑酮的抗药性监测.植物保护,2008,34(6):74-77.
3.曹学仁,周益林,段霞瑜,等.小麦白粉病有性时期闭囊壳在病害侵染循环中作用的初步研究.植物保护,2010,36(5):151-154.
4.曹亚萍.小麦的起源、进化与中国小麦遗传资源.小麦研究,2008,29(3):1-10.
5.曹远银,迟文娟,张晓蕾,等.2004～2008年东北春麦区小麦白粉病菌种群毒性动态分析.植物保护学报,2009,36(3):213-218.
6.陈利锋,徐敬友,等.农业植物病理学(南方本).北京:中国农业出版,2001,141-147.
7.陈瑞辉,王克荣.我国棉花黄萎病菌的群体遗传.棉花学报,2001,13(4):209-212.
8.单卫星,陈受宜,吴立人,等.中国小麦条锈菌流行小种的RAPD分析.中国农业科学,1995,28:1-7.
9.董金皐.农业植物病理学(北方本).北京:中国农业出版社,2001,56-60.
10.段会军,张彩英,李喜焕,等.基于RAPD、ISSR和AFLP对西瓜枯萎病菌遗传多样性的评价.菌物学报,2008,27(2):267-276.
11.段双科,许育彬,吴兴元.小麦白粉病菌致病毒性和抗病基因及抗病育种研究进展.麦类作物学报,2002,22(2):83-86.
12.段霞瑜,盛宝钦,周益林,向齐君.小麦白粉病菌生理小种的鉴定与病菌毒性的监测.植物保护学报,1998,25(1):31-35.
13.段霞瑜.欧洲小麦白粉菌的毒性监测和抗病基因的利用.植物保护,1994,20(3):36-37.
14.段霞瑜.小麦白粉菌群体多样性DNA分子标记的研究[博士学位论文].北京:中国农业大学,1998.
15.甘丽萍,王生荣.甘肃省中西部小麦白粉菌生理小种RAPD分析.河南农业科学,2009:64-67.
16.甘丽萍.小麦白粉菌RAPD分析及不同白粉菌种间亲缘关系研究[硕士学位论文].兰州:甘肃农业大学,2004.
17.谷守芹,范永山,李坡,等.玉米大斑病菌ISSR反应体系的优化和遗传多样性分析.植物保护学报,2008,35(5):427-432.
18.郭爱国,刘颖超,张风国,等.河北省小麦白粉菌群体毒性组成和小麦品种抗性分析.河北农业大学学报.1992,15(2):4-7.
19.郭小山,熊战之,付佑胜,等.小麦白粉病的发生及综合防治研究.上海农业科技,2006,3:88-89.
20.郭新红.不同倍性鱼类mtDNA及三倍体湘云鲫Sox基因研究[博士学位论文].长沙:湖南师范大学,2004.
21.韩加军,林英任,刘艳兵,等.散斑壳属ISSR-PCR反应条件的优化.微生物学杂志,2008,28:20-23.
22.何家泌,何文兰.小麦白粉病及其防治: II小麦白粉病的病原菌.河南农业科学,1998,2:17-19.
23.何家泌,宋玉立,张忠山,等.小麦白粉病及其防治: Ⅰ小麦白粉病的分布、症状和危害.河南农业科学,1998,1:17-18.
24.何家泌.小麦白粉病及其防治.河南农业科学,1998,1:17-18.
25.何世川,林代福,庞纯翠,等.贵州小麦白粉病初侵染源的探讨.植物保护学报,1984,11(3):214-216.
26.何月秋, Heil, Robert S,等.稻瘟病菌变异菌株的AFLP分析.菌物系统,2002,21(3):363-369.
27.黄代新,张林,吴梅筠.单核苷酸多态性研究进展.法医学杂志,2001,17(2):122-125.
28.霍云凤,曹丽华,段霞瑜,等.河南省西部山区小麦白粉菌群体遗传多样性分析.植物保护学报,2010,37(6):481-486.
29.霍治国,刘万才.气候异常与中国小麦白粉病灾害流行关系的研究.自然灾害学报,2002,11(2):85-90.
30.霍治国,刘万才.试论开展中国农作物病虫害危害流行的长期气象预测研究.自然灾害学报,2000,9(1):117-121.
31.季宏平,孟庆林,王芊,等.黑龙江省小麦白粉病菌毒性结构和毒性频率研究.黑龙江农业科学,2007,(3):49-51.
32.贾少锋.小麦遗传多样性对白粉病及其致病菌群体的影响[博士学位论文].福州:福建农林大学,2007.
33.姜占发.棉花黄萎病菌基因组ISSR分子指纹分析[硕士学位论文].郑州:河北农业大学,2002.
34.蒋春先,齐会会,孙明阳,武俊杰,张云慧,程登发.2010年广西兴安地区稻纵卷叶螟发生动态及迁飞轨迹分析.生态学报.2011,31(21):6495-6504.
35.李伯宁.基于GIS的小麦白粉病的越夏和越冬区划[硕士学位论文].北京:中国农业科学院,2008.
36.李川,刘海英,范永山,李聪文.植物病原真菌群体遗传学研究进展.河北农业大学学报,2003,26:177-179.
37.李光博,曾士迈,李振歧.小麦病虫草鼠害综合防治.北京:中国农业科技出版社,1990,226-237.
38.李海莲.茄子黄萎病病原菌鉴定及其ISSR分子指纹分析[硕士学位论文].南京:南京农业大学,2005.
39.李继平,金社林,曹世勤,陈怡蓉,金明安.2003.小麦抗白粉病基因在甘肃的有效性及评价.植物保护学报,30(1):30-34.
40.李继平,金社林,史延春,等.小麦白粉病菌有性时期在侵染循环中的作用.植物保护,2000,26(3):14-16.
41.李隆业,黄元江.小麦白粉菌群体的毒性基因研究.植物病理学报,1992,22(1):55-58.
42.李亚红.豫、鄂、渝三省（市）小麦白粉菌群体遗传结构研究[硕士学位论文].郑州:河南农业大学,2011.
43.刘帆,骆勇,马占鸿.我国小麦条锈菌主要流行小种CY32的SSR标记.北京:中国植物病理学会2007年学术年会论文集,2007.
44.刘万才,邵振润.我国小麦白粉病大区流行的气候因素分析.植保技术与推广,1998,18(1):3-7.
45.刘万才,邵振润.我国小麦白粉病发生演替的成因及趋势浅析.植保技术与推广,1995,(6):7-8.
46.刘孝坤.我国小麦白粉病研究进展.农牧科技情报,1989,1:1-6.
47.刘逸卿.小麦白粉菌无性世代在侵染循环中的作用.植物病理学报,1985,15(3):191-192.
48.龙增栋,何庆才,廖玉梅.小麦白粉病抗源贵农21在育种中的利用.贵州农业科学,1998,26(1):17-20.
49.鲁国东,王宝华,赵志颖,等.福建稻瘟病菌群体遗传多样性RAPD分析.福建农林大学学报,2000,29(1):54-59.
50.陆遥,付洁,毛岚,等.英法两国不同生理小种苹果黑星病菌遗传多样性的SSR分析.西北农林科技大学学报(自然科学版),2008,36(6):170-174.
51.罗琼.小麦白粉菌群体多样性RAPD分析及无毒性遗传分析[硕士学位论文].北京:中国农业科学院,2002.
52.马志强,刘国容,张小凤,等.小麦白粉病对三唑酮抗药性的监测方法.南京农业大学报,1996,19:38-41.
53.毛岚,宋培玲,杨家荣.陕西棉花黄萎病菌致病力分化及其遗传多样性.植物保护学报,2009,36(1):27-31.
54.齐会会,张云慧,蒋春先,孙明阳,杨秀丽,程登发.广西东北部稻区白背飞虱早期迁入虫源分析.中国农业科学,2011,44(16):3333-3342.
55.沈瑛, Frouin J,何月秋,等.湖南烟溪病圃稻瘟病菌的有性态及微卫星标记的遗传多样性分析.中国水稻科学,2004,18:262-268.
56.沈瑛,朱培良,袁筱萍.我国稻瘟病菌的遗传多样性及其地理分布.中国农业科学,1996,29(4):39-46.
57.盛宝钦,段霞瑜,周益林,等.小麦白粉病菌对小麦属不同种小麦的寄生专化性研究.中国植物保护研究进展.北京:科技出版社,1996,8.
58.盛宝钦和段霞瑜.我国小麦白粉病大区流行病菌远距离传播区系刍议.中国有害生物综合治理论文集.北京:中国农业科技出版社,1996,380-384.
59.盛宝钦,向齐君,段霞瑜等.1991-1992我国小麦白粉病生理小种的变异动态.植物病理学报,1995,(2):116.
60.盛宝钦,向齐君,段霞瑜等.我国小麦白粉病小种毒力变异动态简报.植物保护,1995,21(1):
4.
61.盛宝钦,卓跃楠.我国小麦白粉病发生分布规律及防治对策.中国植物保护研究进展.北京:科学技术出版社,1996,182-187.
62.石磊岩,王莉梅.北方棉区黄萎病菌RAPD分析.植物保护,1997,23(5):3-7.
63.石琳.川、甘、陕三省小麦白粉菌的群体遗传结构研究[硕士学位论文].长春:吉林农业大学,2011.
64.史亚千,王保通,李强,等.陕西省小麦白粉菌毒性结构及主栽小麦品种抗性基因的初步分析.麦类作物学报,2009,29(4):706-711.
65.孙黛珍,王曙光,成志芳.小麦抗白粉病分子育种研究进展.山西农业大学学报(自然科学版),2004,24(2):199-203.
66.唐玉兰,刘泉姣,刘青春.山东省小麦白粉菌类型及群体毒性基因分析.山东农业科学,1995,3:34-36.
67.汪登强,危起伟,王朝明,等.13种鲟形目鱼类线粒体DNA的PCR-RFLP分析.中国水产科学,2005,12(4):383-389.
68.王海光,杨小冰,马占鸿.基于HYSPLIT-4模式的小麦条锈病菌远程传播研究.中国农业大学学报,2010,15(5):55-64.
69.王海光,杨小冰,马占鸿.应用HYSPLIT-4模式分析小麦条锈病菌远程传播事例.植物病理学报,2009,39(2):183-193.
70.王金利,秦国夫,贺伟,等.葡萄座腔菌属及其相关真菌的系统学研究进展.中国森林病虫,2003,22:32-36.
71.王丽,陈鹏,周益林,等.2009年我国部分麦区小麦白粉菌群体对三唑酮和嘧菌酯的敏感性测定.植物病理学报,2011,41(6):654-658.
72.王龙,王生荣,甘丽萍.甘肃中西部春小麦白粉病菌群体毒性分析.西北农业学报,2005,14(1):106-110.
73.王萌.小麦白粉病菌SSR标记的开发及其在群体遗传多样性中的应用[硕士学位论文].北京:中国农业大学,2010.
74.王沁.自然选择和中性说.高等函授学报（自然科学版）,1999,5:40-43.
75.王锡锋,刘红彦,何文兰,等.河南小麦白粉病秋季菌源毒性结构的初步分析.植物保护,1991,17(5):2-4.
76.王宗华,鲁国东,谢联辉,等.对植物病原真菌群体遗传研究范畴及其意义的认识.植物病理学报,1998,28(1):5-9.
77.魏松红,杨家书,等.东北春麦区小麦白粉病菌生理小种鉴定及其RAPD分析.吉林农业大学学报,2001,23(2):35-37.
78.吴先华,罗培高,姜本菊,等.小麦抗白粉病基因的定位及其在育种中的应用研究进展.中国农学通报,2005,22(5):346-351.
79.吴小芹.林木病原真菌的群体分化研究.林业科学研究,2000,13(4):423-430.
80.武英鹏,原宗英,李艳芳,等.山西省不同生态区小麦白粉病菌毒性监测研究.中国生态农业学报,2005,13(2):62-64.
81.夏烨,周益林,段霞瑜,等.2002年部分麦区小麦白粉病菌对三唑酮的抗药性监测及苯氧菌酯敏感基线的建立.植物病理学报,2005,35:74-78.
82.向梅梅.植物病原真菌分子生物学研究进展.仲恺农业技术学院学报,2001,14(4):52-58.
83.向齐军,周益林,段霞瑜,盛宝钦.我国小麦白粉菌的遗传变异及其与育种的关系.中国植物保护研究进展.北京:科学技术出版社,1996,8.
84.肖仲久,蒋选利,李小霞,等.基于RAPD对贵州省小麦白粉菌的遗传多样性评价.湖北农业科学,2009,48(4):769-772.
85.肖仲久,徐如宏,任明见,等.贵州小麦白粉菌RAPD分析.山地农业生物学报,2006,25(6):501-505.
86.徐志,梅丽红,李志英,等.利用AFLP分子标记和无毒基因构建小麦白粉菌遗传连锁图谱.植物病理学,2009,39(1):16-22.
87.徐志.我国部分麦区小麦白粉病菌群体遗传多样性分析[硕士学位论文].福州:福建农林大学,2010.
88.许利强,李涛,王克荣.利用ISSR分析栗疫病菌群体遗传多样性.农业生物技术学报,2008,16(4):701-705.
89.薛飞,翟雯雯,段霞瑜,等.小麦地方品种小白冬麦抗白粉病基因分子标记.作物学报,2009,35(10):1806-1811.
90.薛飞.小麦农家品种抗白粉病基因分子标记分析[硕士学位论文].杨凌:西北农林科技大学,
2009.
91.杨定斌,刘孝坤,宋凤仙,等.北京地区小麦白粉病初侵染源的研究.植物保护学报,1996,23(4):300-304.
92.杨立军,向礼波,曾凡松,等.湖北麦区小麦白粉病菌毒性结构分析.植物保护,2009,35(5):76-79.
93.杨鹏,张荣,段霞瑜,等.2008年我国主要麦区白粉菌群体对三唑酮和喹氧灵的敏感性监测.植物病理学报,2010,40(4):404-410.
94.杨志辉,朱杰华,张凤国.中国马铃薯晚疫病菌AFLP遗传多样性分析.菌物学报,2008,27(3):351-359.
95.姚国胜,王俊山,杨英茹,等.河北省和黑龙江省马铃薯晚疫病菌SSR基因型分析.科技导报,2008,26(5):35-39.
96.余仲东,张刚龙,曹支敏.病原真菌种内群体遗传分化研究现状与技术.西北林学院学报,2002,17(4):66-72.
97.曾士迈,孙平.华北西北长江中下游小麦条锈病流行区划的研究//赵美琦.麦田植保系统工程的研究.北京:北京农业大学出版社,1995:125-133.
98.张宏伟.小麦白粉病的危害及综合防治方法.今日农药,2009,03:42.
99.张晓蕾,曹远银,孙芳,等.东北春麦区2006-2007年小麦白粉病菌群体毒性监测.植物保护,2008,34(3):29-32.
100.张艺萍,罗文富,杨艳丽.马铃薯和番茄晚疫病菌全基因组DNA的RAPD多态性分析.云南农业大学学报,2007,22(3):352-357.
101.张跃进,姜玉英,冯晓东,等.2009年全国农作物重大病虫害发生趋势.中国植保导刊,2009,29(3):33-35.
102.张云慧,陈林,程登发,姜玉英,吕英.草地螟2007年越冬成虫迁飞行为研究与虫源分析.昆虫学报,2008,51(7):720-727.
103.张云慧,程登发,姜玉英,张跃进,孙京瑞.北京地区越冬代旋幽夜蛾迁飞的虫源分析.中国农业科学,2010,43(9):1815-1822.
104.张志德,李振岐.小麦白粉菌有性时期的寿命、成熟和作用.西北农业大学学报,1986,14(2):52-61
105.赵广才.中国小麦种植区划研究（一）.麦类作物学报,2010,30(5):886-895.
106.郑冰蓉,张亚平.云南倒刺鲃mtDNA D-loop序列的遗传多样性研究.水利渔业,2002,22(3):15-16.
107.郑文明,陈受宜,康振生,等.甘肃天水地区小麦条锈菌自然群体DNA指纹分析.菌物学报,2005,24(2):199-206.
108.郑文明,康振生,蒋士君,等.小麦条锈菌分子生态学研究进展.应用生态学报,2008,19:681-685.
109.朱海荣.我国部分麦区小麦白粉病菌的遗传多样性研究[硕士学位论文].沈阳:沈阳农业大学,2009.
110.朱建祥.我国小麦白粉病逐年加重的原因分析及对策.安徽农业科学,1992,20(2):174-180.
111.朱文华,任明见,张卫兵,等.小麦白粉菌有性和无性世代菌源毒性结构比较.贵州农学院学报,1997,16(2):27-32.
112.朱振东.小麦抗白粉病新基因的发现[博士学位论文].北京:中国农业科学院,2003.
113.庄巧生,主编.中国小麦品种改良及系谱分析.北京:中国农业出版社,2003,469-487.
114.邹亚飞,简桂良,马存,等.棉花黄萎病菌致病型的AFLP分析.植物病理学报,2003,33(2):135-141.
115. Abu-El Samen F. M., Secor G. A., Gudmestad N. C.. Genetic variation among asexual progeny ofPhytophthora infestans detected with RAPD and AFLP markers. Plant Pathology,2003,52:314-325.
116. Allendorf F. Isolation, gene flow and genetic differentiation among populations. Genetics andConservation,1983,51-65.
117. Anderson N. O.. The distribution of the genus Lilium with reference to its evolution. Herbertia,l986,42: l-18.
118. Aranishi F., Okimoto T., Izumi S.. Identification of gadoid species (Pisces, Gadidae) by PCR-RFLPanalysis [J]. J Appl Genet,2005,46(1):69-73.
119. Bakonyi J., Laday M., Dula T., et al. Characterisation of isolates of Phytophthora infestans fromHungary [J]. European Journal of Plant Pathology,2002,108:139-146.
120. Ben Ari G., Zenvirth D., Sherman A., et al. Application of SNPs for assessing biodiversity andphylogeny among yeast strains. Heredity,2005,95:493-501.
121. Bennett F. G. A. Resistance to powdery mildew in wheat: a review of its use in agriculture andbreeding programmes. Plant Pathology,1984,33:279-300.
122. Brewer M. T. and Milgroom M. G.. Phylogeography and population structure of the grape powderymildew fungus, Erysiphe necator, from diverse Vitis species. BMC Evolutionary Biology,2010,10:
268.
123. Brown J. K. M. and Hovm ller M. S.. Aerial dispersal of pathogens on the global and continentalscales and its impact on plant disease. Science,2002,297:537-541.
124. Brown J. K. M. and Wolfe M.S.. Structure and evolution of a population of Erysiphe graminis f. sp.hordei. Plant Pathol.,1990,39:376-390.
125. Brown J. K. M.. The choice of molecular marker methods for population genetic studies of plantpathogens. New Phytologist,1996,133:183-195.
126. Brown, J. K. M., Jessop, K. C., and Rezanoor, H. N. Genetic uniformity in barley and its powderymildew pathogen. Proc. R. Soc. Lond. B,1991,246:83-90.
127. Carder J. H., Barbara D. J.. Molecular variation and restriction fragment length polymorphisms(RFLPs) within and between six species of Verticillium. Mycological Research,1991,95(8):935-942.
128. Carter J. P., Rezanoor H. N., Desjardins A. E. and Nicholson P.. Variation in Fusariumgraminearum isolates from Nepal associated with their host of origin Plant Pathology,2000,49:452-46.
129. Chen X. M., Line R. F., Leung H.. Relationship between virulence variation and DNApolymorphism in Puccinia striiformis. Phytopathology,1993,83:1489-1497.
130. Chow S., Okamoto H., Uozumi, et al. Genetic stock structure of the swordfish (Xiphias gladius)inferred by PCR-RFLP analysis of the mitochondrial DNA control region. Marine Biology,1997,127:359-367.
131. Collins F. S., Guyer M. S., Chak ravarti A.. Variations on a theme: cataloging human DNAsequence variation. Science,1997,278:1580-1581.
132. DE VALLAVIEILLE-POPE. Racial diversity and complexity in regional populations of E rysip heg raminis f. sp. hordei in France over a5-year period. Plant Pathology,1993,42:443-464.
133. Enjalbert J., Duan X., Leconte M., et al. Genetic evidence of local adaptation of wheat yellow rust(Puccinia striiformis f.sp. tritici) within France. Molecular Ecology,2005,14(7):2065-2073.
134. Flor H. H.. Current status of the gene-for-gene concept. Annual Review of Phytopathology,1971,9:275-276.
135. Forster H., Oudemans P., Coffey M.. Mitochondrial and nuclear DNA diversity within six speciesof Phytophthora. Experimental mycology (USA),1989,14:18-31.
136. Francis S. C., Lisa D. B., Aravinda C.. A DNA polymorphism discovery resource for research onhuman genetic variation. Genome Res,1998,8:1229-1231.
137. Fu Y. X. Statistical tests of neutrality of mutations against population growth, hitchhiking andbackground selection. Genetics.1997,147(2):915-925.
138. Gale L. R., Chen L. F., Hernick C. A., Takamura K. and Kistler H. C.. Population analysis ofFusarium graminearum from wheat fields in eastern China. Phytopathology,2002,92:1315-1322.
139. Gianni L., David M. C., Alan M. M., et al.. Population genomics of domestic and wild yeasts.Nature,2009,458:337-341.
140. Gilchrist E. J., Haughn G. W., Ying C. C., et al.. Use of ecotilling as an efficient SNP discovery toolto survey genetic variation in wild populations of Populus trichocarpa. Mol Ecol,2006,15(5):1367-1378.
141. Goldstein D. B.. Islands of linkage disequilibrium. Nat Genet,2001,29:109-111.
142. Grodzicker T., Williams J., Sharp P., et al.. Physical mapping of temperature sensitive mutations ofadenovirus. Cold Spring Habor Symposia on Quantitative Biology,1974,39:439-446.
143. Hamer J. E., Farrall L., Orbach J., et al.. Host species-specific conservation of a family of repeatedDNA sequences in the genome of a fungal plant pathogen. Proc Natl Acad Sci USA,1989,86:9981-9985.
144. Han Y., Duan Y H, et al.. Genetic structure of three populations of Oxya chinensis in Shanxi, China.Zool Res.2002,23(1):76-80.
145. Harpending H. C., M. A. Batzer, et al.. Genetic traces of ancient demography. Proceedings of theNational Academy of Sciences.1998,95(4):1961-1967.
146. Hatira T., Saadet B., Hasan H. D., et al.. A multigene molecular phylogenetic assessment of truemorels (Morchella) in Turkey. Fungal Genetics and Biology,2010,47:672-682.
147. Hovm ller M. S.&Justesen, A. F.. Rates of evolution of avirulence phenotypes and DNA markersin a northwest European population of Puccinia striiformis f. sp. tritici. Molecular Ecology,2007,16,4637–4647.
148. Hovmoller M. S., Justesen A. F., Brown J. K. M.. Clonality and long-distance migration ofPuccinia striiformis in NW-Europe. Plant Pathol,2002,51:24-32.
149. Inuma T., Khodaparast S. A., Takamatsu S.. Multilocus phylogenetic analyses within Blumeriagraminis, a powdery mildew fungus of cereals. Molecular Phylogenetics and Evolution,2007,44,741-751.
150. Jevtic R., Pribakovic M., Stojanovic S., et al.. Screening the virulence of Erysiphe graminis DC.Ex Merat f. sp. tritici Em. Marchal in mobile nurseries. Plant Prot.1991,42:21-31.
151. Joseph S., Joshua A. S., Douglas M. R., et al.. Comprehensive polymorphism survey elucidatespopulation structure of S. cerevisiae. Nature,2009,458:342-345.
152. Kanazin V., Talbert H., See D., et al.. Discovery and assay of single-nucleotide polymorphisms inbarley (Hordeum vulgare). Plant Mol Biol,2002,48:529-537.
153. Karen H., Katherine F. L., Donald H. P.. Evolutionary relationships of the cup-fungus genus Pezizaand Pezizaceae inferred from multiple nuclear genes: RPB2, β-tubulin, and LSU rDNA. MolecularPhylogenetics and Evolution,2005,36:1-23.
154. Kimura M.. Evolutionary rate at the molecular level. Nature,1968,217:624-626.
155. Kimura M.. The neutral theory of molecular evolution. Cambridge University Press, London.1983.
156. Kinoshita A., Sasaki H., Nara K.. Phylogeny and diversity of Japanese truffles (Tuber spp.)inferred from sequences of four nuclear loci. Mycologia,2011, DOI:10.3852/10-138.
157. Koltin Y. and Kenneth R.. The role of the sexual stage in the over-summering of Erysiphe graminisDC. f. sp. hordei Marchal under semiarid conditions. Annals of Applied Biology,1970,65,263-268.
158. Kota R., Varshney R. K., Thiel T., et al.. Generation and comparison of EST-derived SSRs andSNPs in barley (Hordeum vulgare L.). Hereditas,2001,135:145-151.
159. Krutovsky K. V., Neale D. B.. Nucleotide diversity and linkage disequilibrium in cold-hardiness-and wood quality-related candidate genes in douglas fir. Genetics,2005,171(4):2029-2041.
160. Lander E. S.. The new genomics: global views of biology. Science,1996,274:536-539.
161. Leath S. and Murphy J. P., Virulence genes of the wheat powdery mildew fungus, Erysiphegraminis f. sp. tritici in North Carolina. Plant Dis.1985,69:905.
162. Leath S.. Wheat powdery mildew in the USA: Status of pathogen virulence and host resistance.Integrated Control of Cereal Mildews: Virulence Patterns and Their Change.1991,22-32.
163. Leila M.C.. Variability of the wheat powdery mildew pathogen Blumeria graminis f.sp. tritici inthe2003crop season. Fitopatologia Brasileira.2005,30(4):420-422.
164. Limpert E., Felsenstein F. G., and Andrivon D.. Analysis of virulence in populations of wheatpowdery mildew in Europe. J. Phytopathol.1987,120:1-8.
165. Mahuku G., Peters R. D., Plattff H. W.. Random amplication polymorphic DNA (RAPD) analysisof Phytophthora infestans isolates collection in Canada during1994-1996. Plant Pathology,2000,49:252-260
166. Majer D., Mithen R., Lewis B., et al.. The use of AFLP fingerprinting for the detection of geneticvariation in fungi. Mycological Research (United Kingdom),1996,100:1107-1111.
167. Marshall. Snipping away at genome patenting. Science,1997,277(19):1752-1753.
168. McDermott J. M., Brandle U., Dutly F., et al.. Genetic variation in powdery mildew of barley:Development of RAPD, SCAR and VNTR markers. Phytopathology.1994,84(11):1316-1321.
169. McDonald B. A. and Linde C.. Pathogen population genetics, evolutionary potential and durableresistance. Annu. Rev. Phytopathol.2002,40,349–379.
170. McDonald B. A. and Linde C.. The population genetics of plant pathogens and breeding strategiesfor durable resistance. Euphytica2002,124:163-180.
171. McDonald B. A. and McDermott J. M.. The population genetics of plant pathogenic fungi.BioScience1993,43:311-319.
172. McDonald B.A.. Population genetics of plant pathogenic fungi. Encyclopedia of Plant and Cropscience,2007,1046-1048.
173. McDonald B.A.. The population genetics of fungi: Tools and techniques. Phytopathology1997,87,448–453.
174. Michael R., Carrie S. T., Briana L. G., et al.. Genomic patterns of nucleotide diversity in divergentpopulation of U.S. weedy rice. BMC Evolutionary Biology,2010,10:180.
175. Namuco L. O., Coffman W. R., Bergstrom G. C., et al.. Virulence spectrum of the Erysiphegraminis f. sp. tritici population in New York. Plant Dis.1987,71:539-541.
176. Nei M.. Molecular Evolutionary Genetics. New York: Columbia University Press,1987,176-192.
177. Niewoehner A. S. and Leath S.. Virulence of Blumeria graminis f. sp. tritici on winter wheat in theeastern United States. Plant Dis.1998,82:64-68.
178. O’Donnell K., Ward T. J., Aberra D., et al.. Multilocus genotyping and molecular phylogeneticsresolve a novel head blight pathogen within the Fusarium graminearum species complex fromEthiopia. Fungal Genetics and Biology,2008,45:1514-1522.
179. O'Dell M., Wolfe M. S., Flavell R. B., et al.. Molecular variation in populations of Erysiphegraminis on barley, oats and rye. Plant Pathology.1989,38(3):340-351.
180. Okoli C. A. N., Carder J. H., Barbara D. J.. Restriction fragment length polymorphisms (RFLPs)and the relationships of some host-adapted isolats of Verticillium dahliae. Plant Pathology,1994,43:33-40
181. Olivieri I D Couvet, P H Gouyon. Trends Evolution,1990,5:207-210.
182. Pan Z, Yang X B, Pivonia S, et al.. Long-term predietion of soybean rust entry into the continentalUnited States. Plant Disease,2006,90:840-846.
183. Parks R., Carbone I., Murphy J. P., and Cowger C.. Population genetic analysis of an eastern U.S.wheat powdery mildew population reveals geographic subdivision and recent common ancestrywith U.K. and Israeli populations. Phytopathology,2009,99,840-849.
184. Parks R., Carbone I., Murphy J. P., Marshall D., and Cowger C.. Virulence structure of the easternU.S. wheat powdery mildew population. Plant Dis.2008,92:1074-1082.
185. Peakall R. and Smouse P.E.. GENALEX6: genetic analysis in Excel. Population genetic softwarefor teaching and research. Molecular Ecology Notes6,2006,288-295.
186. Persaud R. R., Lipps P. E.. Virulence genes and virulence gene frequencies of Blumeria graminisf.sp. tritici in Ohio. Plant Disease,1995,79:494-498.
187. Qu B., Li H. P., Zhang J. B., Xu Y. B., Huang T., Wu A. B., Zhao C. S., Carter J., Nicholson P. andLiao Y. C., Geographic distribution and genetic diversity of Fusarium graminearum and F.asiaticum on wheat spikes throughout China. Plant Pathology,2008,57:15-24.
188. Ramsay J. R., Multani D. S., Lyon B. R., RAPD-PCR identification of Verticillium dahliaeisolateswith differential pathogenicity on cotton. Aust J Agric Res,1996,47:681-693
189. Rashmi P., Amita C., Prija P., et al. Single nucleotide polymorphism in the genes of mce1andmce4operons of Mycobacterium tuberculosis: analysis of clinical isolates and tandard referencestrains. BMC Microbiology,2011,11:41.
190. Rosenberg N. A., and Nordborg M., Genealogical trees, coalescent theory and the analysis ofgenetic polymorphisms. Nat. Rev. Genet.2002,3:380-390.
191. Rosendahl S., Talor J. W., Development of multiple genetic markers for studies of genetic variationin arbuscular mycorrhiazl fungi using AFLP. Molecular Ecology,1997,(6):821-829.
192. Rousset F.1997. Genetic differentiation and estimation of gene flow from F-statistics underisolation by distance. Genetics,145:1219-1228.
193. Schaal B. A., Measurement of gene flow in Lupinus texensis. Nature,1980,284:450-451.
194. Shan W. X., Chen S.Y., Kang Z.S., et al. Genetic diversity in Puccinia striiformis f. sp triticirevealed by a pathogen genome-specific repetitive sequence. Canadian Journal of Botany,1998,76:587-595.
195. Slatkin M., Gene flow and the geographic structure of natural population. Science,1987,236:787-792.
196. Slovakova T., Svec M., and Miklovicova M., Do geographical barriers play any role in isolation ofpowdery mildew populations?. Biologia (Bratislava).2004,59:121-126.
197. Stephen B., Goodwin S., Clonal diversity and genetic differentiation of Phytophthora infestanspopulations in Northern and Central Mexico. Phytopathology,1992,82(9):955-961.
198. Tajima F. Statistical Method for Testing the Neutral Mutation Hypothesis by DNA Polymorphism.Genetics.1989,123(3):585-595.
199. Tamura, K., J. Dudley, et al. MEGA4: Molecular Evolutionary Genetics Analysis (MEGA)Software Version4.0. Molecular Biology and Evolution.2007,24(8):1596-1599.
200. Tavare S., Line-of-descent and genealogical processes and their applications in population geneticsmodels. Theor. Popul. Biol.1984,26:119-164
201. Templeton A. R., Nested clade analyses of phylogeographic data: Testing hypotheses about geneflow and population history. Mol. Ecol.1998,7:381-397.
202. Templeton A. R., Routman E., and Philips C. A., Separating population structure from populationhistory: A cladistic analysis of the geographical distribution of mitochondrial DNA haplotypes inthe tiger salamander, Ambystoma tigrinum. Genetics,1995,140:767-782.
203. Thorsten H., Lumbsch N., Wirtz R. L., et al. Higher level phylogenetic relationships ofeuascomycetes (Pezizomycotina) inferred from a combined analysis of nuclear and mitochondrialsequence data. Mycological Progress,2002,1(1):57-70.
204. Troch V., Audenaert K., Bekaert B., Hofte M. and Haesaert G., Phylogeography and virulencestructure of the powdery mildew population on its ‘new’ host triticale. BMC Evolutionary Biology,2012,12,76.
205. Vos P., Hogers R., Bleeker M., et al. AFLP: a new technique for DNA fingerprinting. Nucleic acidsresearch,1995,23:4407-4414.
206. Wang C.H., Li S.F., Genetic variability and relationships in mitochondrial DNA COⅡgenesequence of red common carps in China. Acta Genetica Sinica,2004,31(11):1226-1231.
207. Wang D.G., Fan J.B., Siao C., et al. Large-scale identification, mapping, and genotyping of singlenucleotide polymorphisms in the human genome. Science,1998,280:1077-1082.
208. Wang S.L., Sha Z.X., Tad S.S., et al. Quality assessment parameters for EST-derived SNPs fromcatfish. BMC Genomics,2008,9:45-50.
209. Welsh J. and McClelland M., Fingerprinting genomes using PCR with arbitraryprimers. Nucleic Acids Research,1990,18:7213-7218.181.
210. Whitlock M C, McCauley D E. Indirect measures of gene flow and migration: Fst1/(4Nm+1).Heredity,1999,82:117-125.
211. Williams J., Kubelik A., Livak K., et al. DNA polymorphisms amplified by arbitrary primers areuseful as genetic markers. Nucleic acids research,1990,18:6531-6535.
212. Wolfe M. S., Schwarzbach E., Patterns of race changes in powdery mildews. Ann Rev Phytopathol,1978,16:159-180.
213. Wolfe M. S., The use of virulence analysis in cereal mildews. Phytopathol Z,1975,82:297-307.
214. Wright S., Evolution in Mendelian populations. Genetics,1931,16:97-159.
215. Wright S., The genetical structure of population. Annual Eugenetics,1951,15:323-354.
216. Wyand R. A. and Brown J. K. M., Genetic and forma specialis diversity in Blumeria graminis ofcereals and its implications for host-pathogen co-evolution. Molecular Plant Pathology,2003,4(3),187-198.
217. Xiao M. G., Song F. J., Jiao J. F., Wang X. M., Xu H. X., Li H. J.. Identification of the gene Pm47on chromosome7BS conferring resistance to powdery mildew in the Chinese wheat landraceHongyanglazi. Theoretical and Applied Genetics,2013,126:1397-1403.
218. Yang J., Wang B., Li G., Bi Y.,&Yuan Z., Wheat stripe rust epidemic and virulence of Pucciniastriiformis f. sp tritici in China in2002. Plant Disease,2004,88,896–904.
219. Yeh F. C., Yang R. C., Boyle T. B. J., POPGENE, the user-friendly share are for population geneticanalysis. Molecular Biotechnology Center,1997,24:112-118.
220. Zabeau M., Vos P., Selective restriction fragment amplification: a general method for DNAfingerprinting. European patent application,1993,92:4026-4029.
221. Zeller K. A., Bowden R. L. and Leslie J. F., Population differentiation and recombination in wheatscab populations of Gibberella zeae from the United States. Molecular Ecology,2004,13:563-571.
222. Zeng S. M. And Luo Y., Long-distance spread and interregional epidemics of wheat stripe rust inChina. Plant Disease,2006,90,980–988.
223. Zhou H., Li D.Q., Zhang Y.G., et al. Study on mitochondrial DNA genetic diversity of TibetanAntelope. Genetic,2006,28(3):299-305.
224. Zietkiewicz E., Rafalski A., Labuda D., Genome fingerprinting by simple sequence repeat(SSR)-anchored polymerase chain reaction amplification. Genomics,1994,20:176-183.
2.曹学仁,赵文娟,周益林,等.2007年我国部分麦区小麦白粉菌对三唑酮的抗药性监测.植物保护,2008,34(6):74-77.
3.曹学仁,周益林,段霞瑜,等.小麦白粉病有性时期闭囊壳在病害侵染循环中作用的初步研究.植物保护,2010,36(5):151-154.
4.曹亚萍.小麦的起源、进化与中国小麦遗传资源.小麦研究,2008,29(3):1-10.
5.曹远银,迟文娟,张晓蕾,等.2004～2008年东北春麦区小麦白粉病菌种群毒性动态分析.植物保护学报,2009,36(3):213-218.
6.陈利锋,徐敬友,等.农业植物病理学(南方本).北京:中国农业出版,2001,141-147.
7.陈瑞辉,王克荣.我国棉花黄萎病菌的群体遗传.棉花学报,2001,13(4):209-212.
8.单卫星,陈受宜,吴立人,等.中国小麦条锈菌流行小种的RAPD分析.中国农业科学,1995,28:1-7.
9.董金皐.农业植物病理学(北方本).北京:中国农业出版社,2001,56-60.
10.段会军,张彩英,李喜焕,等.基于RAPD、ISSR和AFLP对西瓜枯萎病菌遗传多样性的评价.菌物学报,2008,27(2):267-276.
11.段双科,许育彬,吴兴元.小麦白粉病菌致病毒性和抗病基因及抗病育种研究进展.麦类作物学报,2002,22(2):83-86.
12.段霞瑜,盛宝钦,周益林,向齐君.小麦白粉病菌生理小种的鉴定与病菌毒性的监测.植物保护学报,1998,25(1):31-35.
13.段霞瑜.欧洲小麦白粉菌的毒性监测和抗病基因的利用.植物保护,1994,20(3):36-37.
14.段霞瑜.小麦白粉菌群体多样性DNA分子标记的研究[博士学位论文].北京:中国农业大学,1998.
15.甘丽萍,王生荣.甘肃省中西部小麦白粉菌生理小种RAPD分析.河南农业科学,2009:64-67.
16.甘丽萍.小麦白粉菌RAPD分析及不同白粉菌种间亲缘关系研究[硕士学位论文].兰州:甘肃农业大学,2004.
17.谷守芹,范永山,李坡,等.玉米大斑病菌ISSR反应体系的优化和遗传多样性分析.植物保护学报,2008,35(5):427-432.
18.郭爱国,刘颖超,张风国,等.河北省小麦白粉菌群体毒性组成和小麦品种抗性分析.河北农业大学学报.1992,15(2):4-7.
19.郭小山,熊战之,付佑胜,等.小麦白粉病的发生及综合防治研究.上海农业科技,2006,3:88-89.
20.郭新红.不同倍性鱼类mtDNA及三倍体湘云鲫Sox基因研究[博士学位论文].长沙:湖南师范大学,2004.
21.韩加军,林英任,刘艳兵,等.散斑壳属ISSR-PCR反应条件的优化.微生物学杂志,2008,28:20-23.
22.何家泌,何文兰.小麦白粉病及其防治: II小麦白粉病的病原菌.河南农业科学,1998,2:17-19.
23.何家泌,宋玉立,张忠山,等.小麦白粉病及其防治: Ⅰ小麦白粉病的分布、症状和危害.河南农业科学,1998,1:17-18.
24.何家泌.小麦白粉病及其防治.河南农业科学,1998,1:17-18.
25.何世川,林代福,庞纯翠,等.贵州小麦白粉病初侵染源的探讨.植物保护学报,1984,11(3):214-216.
26.何月秋, Heil, Robert S,等.稻瘟病菌变异菌株的AFLP分析.菌物系统,2002,21(3):363-369.
27.黄代新,张林,吴梅筠.单核苷酸多态性研究进展.法医学杂志,2001,17(2):122-125.
28.霍云凤,曹丽华,段霞瑜,等.河南省西部山区小麦白粉菌群体遗传多样性分析.植物保护学报,2010,37(6):481-486.
29.霍治国,刘万才.气候异常与中国小麦白粉病灾害流行关系的研究.自然灾害学报,2002,11(2):85-90.
30.霍治国,刘万才.试论开展中国农作物病虫害危害流行的长期气象预测研究.自然灾害学报,2000,9(1):117-121.
31.季宏平,孟庆林,王芊,等.黑龙江省小麦白粉病菌毒性结构和毒性频率研究.黑龙江农业科学,2007,(3):49-51.
32.贾少锋.小麦遗传多样性对白粉病及其致病菌群体的影响[博士学位论文].福州:福建农林大学,2007.
33.姜占发.棉花黄萎病菌基因组ISSR分子指纹分析[硕士学位论文].郑州:河北农业大学,2002.
34.蒋春先,齐会会,孙明阳,武俊杰,张云慧,程登发.2010年广西兴安地区稻纵卷叶螟发生动态及迁飞轨迹分析.生态学报.2011,31(21):6495-6504.
35.李伯宁.基于GIS的小麦白粉病的越夏和越冬区划[硕士学位论文].北京:中国农业科学院,2008.
36.李川,刘海英,范永山,李聪文.植物病原真菌群体遗传学研究进展.河北农业大学学报,2003,26:177-179.
37.李光博,曾士迈,李振歧.小麦病虫草鼠害综合防治.北京:中国农业科技出版社,1990,226-237.
38.李海莲.茄子黄萎病病原菌鉴定及其ISSR分子指纹分析[硕士学位论文].南京:南京农业大学,2005.
39.李继平,金社林,曹世勤,陈怡蓉,金明安.2003.小麦抗白粉病基因在甘肃的有效性及评价.植物保护学报,30(1):30-34.
40.李继平,金社林,史延春,等.小麦白粉病菌有性时期在侵染循环中的作用.植物保护,2000,26(3):14-16.
41.李隆业,黄元江.小麦白粉菌群体的毒性基因研究.植物病理学报,1992,22(1):55-58.
42.李亚红.豫、鄂、渝三省（市）小麦白粉菌群体遗传结构研究[硕士学位论文].郑州:河南农业大学,2011.
43.刘帆,骆勇,马占鸿.我国小麦条锈菌主要流行小种CY32的SSR标记.北京:中国植物病理学会2007年学术年会论文集,2007.
44.刘万才,邵振润.我国小麦白粉病大区流行的气候因素分析.植保技术与推广,1998,18(1):3-7.
45.刘万才,邵振润.我国小麦白粉病发生演替的成因及趋势浅析.植保技术与推广,1995,(6):7-8.
46.刘孝坤.我国小麦白粉病研究进展.农牧科技情报,1989,1:1-6.
47.刘逸卿.小麦白粉菌无性世代在侵染循环中的作用.植物病理学报,1985,15(3):191-192.
48.龙增栋,何庆才,廖玉梅.小麦白粉病抗源贵农21在育种中的利用.贵州农业科学,1998,26(1):17-20.
49.鲁国东,王宝华,赵志颖,等.福建稻瘟病菌群体遗传多样性RAPD分析.福建农林大学学报,2000,29(1):54-59.
50.陆遥,付洁,毛岚,等.英法两国不同生理小种苹果黑星病菌遗传多样性的SSR分析.西北农林科技大学学报(自然科学版),2008,36(6):170-174.
51.罗琼.小麦白粉菌群体多样性RAPD分析及无毒性遗传分析[硕士学位论文].北京:中国农业科学院,2002.
52.马志强,刘国容,张小凤,等.小麦白粉病对三唑酮抗药性的监测方法.南京农业大学报,1996,19:38-41.
53.毛岚,宋培玲,杨家荣.陕西棉花黄萎病菌致病力分化及其遗传多样性.植物保护学报,2009,36(1):27-31.
54.齐会会,张云慧,蒋春先,孙明阳,杨秀丽,程登发.广西东北部稻区白背飞虱早期迁入虫源分析.中国农业科学,2011,44(16):3333-3342.
55.沈瑛, Frouin J,何月秋,等.湖南烟溪病圃稻瘟病菌的有性态及微卫星标记的遗传多样性分析.中国水稻科学,2004,18:262-268.
56.沈瑛,朱培良,袁筱萍.我国稻瘟病菌的遗传多样性及其地理分布.中国农业科学,1996,29(4):39-46.
57.盛宝钦,段霞瑜,周益林,等.小麦白粉病菌对小麦属不同种小麦的寄生专化性研究.中国植物保护研究进展.北京:科技出版社,1996,8.
58.盛宝钦和段霞瑜.我国小麦白粉病大区流行病菌远距离传播区系刍议.中国有害生物综合治理论文集.北京:中国农业科技出版社,1996,380-384.
59.盛宝钦,向齐君,段霞瑜等.1991-1992我国小麦白粉病生理小种的变异动态.植物病理学报,1995,(2):116.
60.盛宝钦,向齐君,段霞瑜等.我国小麦白粉病小种毒力变异动态简报.植物保护,1995,21(1):
4.
61.盛宝钦,卓跃楠.我国小麦白粉病发生分布规律及防治对策.中国植物保护研究进展.北京:科学技术出版社,1996,182-187.
62.石磊岩,王莉梅.北方棉区黄萎病菌RAPD分析.植物保护,1997,23(5):3-7.
63.石琳.川、甘、陕三省小麦白粉菌的群体遗传结构研究[硕士学位论文].长春:吉林农业大学,2011.
64.史亚千,王保通,李强,等.陕西省小麦白粉菌毒性结构及主栽小麦品种抗性基因的初步分析.麦类作物学报,2009,29(4):706-711.
65.孙黛珍,王曙光,成志芳.小麦抗白粉病分子育种研究进展.山西农业大学学报(自然科学版),2004,24(2):199-203.
66.唐玉兰,刘泉姣,刘青春.山东省小麦白粉菌类型及群体毒性基因分析.山东农业科学,1995,3:34-36.
67.汪登强,危起伟,王朝明,等.13种鲟形目鱼类线粒体DNA的PCR-RFLP分析.中国水产科学,2005,12(4):383-389.
68.王海光,杨小冰,马占鸿.基于HYSPLIT-4模式的小麦条锈病菌远程传播研究.中国农业大学学报,2010,15(5):55-64.
69.王海光,杨小冰,马占鸿.应用HYSPLIT-4模式分析小麦条锈病菌远程传播事例.植物病理学报,2009,39(2):183-193.
70.王金利,秦国夫,贺伟,等.葡萄座腔菌属及其相关真菌的系统学研究进展.中国森林病虫,2003,22:32-36.
71.王丽,陈鹏,周益林,等.2009年我国部分麦区小麦白粉菌群体对三唑酮和嘧菌酯的敏感性测定.植物病理学报,2011,41(6):654-658.
72.王龙,王生荣,甘丽萍.甘肃中西部春小麦白粉病菌群体毒性分析.西北农业学报,2005,14(1):106-110.
73.王萌.小麦白粉病菌SSR标记的开发及其在群体遗传多样性中的应用[硕士学位论文].北京:中国农业大学,2010.
74.王沁.自然选择和中性说.高等函授学报（自然科学版）,1999,5:40-43.
75.王锡锋,刘红彦,何文兰,等.河南小麦白粉病秋季菌源毒性结构的初步分析.植物保护,1991,17(5):2-4.
76.王宗华,鲁国东,谢联辉,等.对植物病原真菌群体遗传研究范畴及其意义的认识.植物病理学报,1998,28(1):5-9.
77.魏松红,杨家书,等.东北春麦区小麦白粉病菌生理小种鉴定及其RAPD分析.吉林农业大学学报,2001,23(2):35-37.
78.吴先华,罗培高,姜本菊,等.小麦抗白粉病基因的定位及其在育种中的应用研究进展.中国农学通报,2005,22(5):346-351.
79.吴小芹.林木病原真菌的群体分化研究.林业科学研究,2000,13(4):423-430.
80.武英鹏,原宗英,李艳芳,等.山西省不同生态区小麦白粉病菌毒性监测研究.中国生态农业学报,2005,13(2):62-64.
81.夏烨,周益林,段霞瑜,等.2002年部分麦区小麦白粉病菌对三唑酮的抗药性监测及苯氧菌酯敏感基线的建立.植物病理学报,2005,35:74-78.
82.向梅梅.植物病原真菌分子生物学研究进展.仲恺农业技术学院学报,2001,14(4):52-58.
83.向齐军,周益林,段霞瑜,盛宝钦.我国小麦白粉菌的遗传变异及其与育种的关系.中国植物保护研究进展.北京:科学技术出版社,1996,8.
84.肖仲久,蒋选利,李小霞,等.基于RAPD对贵州省小麦白粉菌的遗传多样性评价.湖北农业科学,2009,48(4):769-772.
85.肖仲久,徐如宏,任明见,等.贵州小麦白粉菌RAPD分析.山地农业生物学报,2006,25(6):501-505.
86.徐志,梅丽红,李志英,等.利用AFLP分子标记和无毒基因构建小麦白粉菌遗传连锁图谱.植物病理学,2009,39(1):16-22.
87.徐志.我国部分麦区小麦白粉病菌群体遗传多样性分析[硕士学位论文].福州:福建农林大学,2010.
88.许利强,李涛,王克荣.利用ISSR分析栗疫病菌群体遗传多样性.农业生物技术学报,2008,16(4):701-705.
89.薛飞,翟雯雯,段霞瑜,等.小麦地方品种小白冬麦抗白粉病基因分子标记.作物学报,2009,35(10):1806-1811.
90.薛飞.小麦农家品种抗白粉病基因分子标记分析[硕士学位论文].杨凌:西北农林科技大学,
2009.
91.杨定斌,刘孝坤,宋凤仙,等.北京地区小麦白粉病初侵染源的研究.植物保护学报,1996,23(4):300-304.
92.杨立军,向礼波,曾凡松,等.湖北麦区小麦白粉病菌毒性结构分析.植物保护,2009,35(5):76-79.
93.杨鹏,张荣,段霞瑜,等.2008年我国主要麦区白粉菌群体对三唑酮和喹氧灵的敏感性监测.植物病理学报,2010,40(4):404-410.
94.杨志辉,朱杰华,张凤国.中国马铃薯晚疫病菌AFLP遗传多样性分析.菌物学报,2008,27(3):351-359.
95.姚国胜,王俊山,杨英茹,等.河北省和黑龙江省马铃薯晚疫病菌SSR基因型分析.科技导报,2008,26(5):35-39.
96.余仲东,张刚龙,曹支敏.病原真菌种内群体遗传分化研究现状与技术.西北林学院学报,2002,17(4):66-72.
97.曾士迈,孙平.华北西北长江中下游小麦条锈病流行区划的研究//赵美琦.麦田植保系统工程的研究.北京:北京农业大学出版社,1995:125-133.
98.张宏伟.小麦白粉病的危害及综合防治方法.今日农药,2009,03:42.
99.张晓蕾,曹远银,孙芳,等.东北春麦区2006-2007年小麦白粉病菌群体毒性监测.植物保护,2008,34(3):29-32.
100.张艺萍,罗文富,杨艳丽.马铃薯和番茄晚疫病菌全基因组DNA的RAPD多态性分析.云南农业大学学报,2007,22(3):352-357.
101.张跃进,姜玉英,冯晓东,等.2009年全国农作物重大病虫害发生趋势.中国植保导刊,2009,29(3):33-35.
102.张云慧,陈林,程登发,姜玉英,吕英.草地螟2007年越冬成虫迁飞行为研究与虫源分析.昆虫学报,2008,51(7):720-727.
103.张云慧,程登发,姜玉英,张跃进,孙京瑞.北京地区越冬代旋幽夜蛾迁飞的虫源分析.中国农业科学,2010,43(9):1815-1822.
104.张志德,李振岐.小麦白粉菌有性时期的寿命、成熟和作用.西北农业大学学报,1986,14(2):52-61
105.赵广才.中国小麦种植区划研究（一）.麦类作物学报,2010,30(5):886-895.
106.郑冰蓉,张亚平.云南倒刺鲃mtDNA D-loop序列的遗传多样性研究.水利渔业,2002,22(3):15-16.
107.郑文明,陈受宜,康振生,等.甘肃天水地区小麦条锈菌自然群体DNA指纹分析.菌物学报,2005,24(2):199-206.
108.郑文明,康振生,蒋士君,等.小麦条锈菌分子生态学研究进展.应用生态学报,2008,19:681-685.
109.朱海荣.我国部分麦区小麦白粉病菌的遗传多样性研究[硕士学位论文].沈阳:沈阳农业大学,2009.
110.朱建祥.我国小麦白粉病逐年加重的原因分析及对策.安徽农业科学,1992,20(2):174-180.
111.朱文华,任明见,张卫兵,等.小麦白粉菌有性和无性世代菌源毒性结构比较.贵州农学院学报,1997,16(2):27-32.
112.朱振东.小麦抗白粉病新基因的发现[博士学位论文].北京:中国农业科学院,2003.
113.庄巧生,主编.中国小麦品种改良及系谱分析.北京:中国农业出版社,2003,469-487.
114.邹亚飞,简桂良,马存,等.棉花黄萎病菌致病型的AFLP分析.植物病理学报,2003,33(2):135-141.
115. Abu-El Samen F. M., Secor G. A., Gudmestad N. C.. Genetic variation among asexual progeny ofPhytophthora infestans detected with RAPD and AFLP markers. Plant Pathology,2003,52:314-325.
116. Allendorf F. Isolation, gene flow and genetic differentiation among populations. Genetics andConservation,1983,51-65.
117. Anderson N. O.. The distribution of the genus Lilium with reference to its evolution. Herbertia,l986,42: l-18.
118. Aranishi F., Okimoto T., Izumi S.. Identification of gadoid species (Pisces, Gadidae) by PCR-RFLPanalysis [J]. J Appl Genet,2005,46(1):69-73.
119. Bakonyi J., Laday M., Dula T., et al. Characterisation of isolates of Phytophthora infestans fromHungary [J]. European Journal of Plant Pathology,2002,108:139-146.
120. Ben Ari G., Zenvirth D., Sherman A., et al. Application of SNPs for assessing biodiversity andphylogeny among yeast strains. Heredity,2005,95:493-501.
121. Bennett F. G. A. Resistance to powdery mildew in wheat: a review of its use in agriculture andbreeding programmes. Plant Pathology,1984,33:279-300.
122. Brewer M. T. and Milgroom M. G.. Phylogeography and population structure of the grape powderymildew fungus, Erysiphe necator, from diverse Vitis species. BMC Evolutionary Biology,2010,10:
268.
123. Brown J. K. M. and Hovm ller M. S.. Aerial dispersal of pathogens on the global and continentalscales and its impact on plant disease. Science,2002,297:537-541.
124. Brown J. K. M. and Wolfe M.S.. Structure and evolution of a population of Erysiphe graminis f. sp.hordei. Plant Pathol.,1990,39:376-390.
125. Brown J. K. M.. The choice of molecular marker methods for population genetic studies of plantpathogens. New Phytologist,1996,133:183-195.
126. Brown, J. K. M., Jessop, K. C., and Rezanoor, H. N. Genetic uniformity in barley and its powderymildew pathogen. Proc. R. Soc. Lond. B,1991,246:83-90.
127. Carder J. H., Barbara D. J.. Molecular variation and restriction fragment length polymorphisms(RFLPs) within and between six species of Verticillium. Mycological Research,1991,95(8):935-942.
128. Carter J. P., Rezanoor H. N., Desjardins A. E. and Nicholson P.. Variation in Fusariumgraminearum isolates from Nepal associated with their host of origin Plant Pathology,2000,49:452-46.
129. Chen X. M., Line R. F., Leung H.. Relationship between virulence variation and DNApolymorphism in Puccinia striiformis. Phytopathology,1993,83:1489-1497.
130. Chow S., Okamoto H., Uozumi, et al. Genetic stock structure of the swordfish (Xiphias gladius)inferred by PCR-RFLP analysis of the mitochondrial DNA control region. Marine Biology,1997,127:359-367.
131. Collins F. S., Guyer M. S., Chak ravarti A.. Variations on a theme: cataloging human DNAsequence variation. Science,1997,278:1580-1581.
132. DE VALLAVIEILLE-POPE. Racial diversity and complexity in regional populations of E rysip heg raminis f. sp. hordei in France over a5-year period. Plant Pathology,1993,42:443-464.
133. Enjalbert J., Duan X., Leconte M., et al. Genetic evidence of local adaptation of wheat yellow rust(Puccinia striiformis f.sp. tritici) within France. Molecular Ecology,2005,14(7):2065-2073.
134. Flor H. H.. Current status of the gene-for-gene concept. Annual Review of Phytopathology,1971,9:275-276.
135. Forster H., Oudemans P., Coffey M.. Mitochondrial and nuclear DNA diversity within six speciesof Phytophthora. Experimental mycology (USA),1989,14:18-31.
136. Francis S. C., Lisa D. B., Aravinda C.. A DNA polymorphism discovery resource for research onhuman genetic variation. Genome Res,1998,8:1229-1231.
137. Fu Y. X. Statistical tests of neutrality of mutations against population growth, hitchhiking andbackground selection. Genetics.1997,147(2):915-925.
138. Gale L. R., Chen L. F., Hernick C. A., Takamura K. and Kistler H. C.. Population analysis ofFusarium graminearum from wheat fields in eastern China. Phytopathology,2002,92:1315-1322.
139. Gianni L., David M. C., Alan M. M., et al.. Population genomics of domestic and wild yeasts.Nature,2009,458:337-341.
140. Gilchrist E. J., Haughn G. W., Ying C. C., et al.. Use of ecotilling as an efficient SNP discovery toolto survey genetic variation in wild populations of Populus trichocarpa. Mol Ecol,2006,15(5):1367-1378.
141. Goldstein D. B.. Islands of linkage disequilibrium. Nat Genet,2001,29:109-111.
142. Grodzicker T., Williams J., Sharp P., et al.. Physical mapping of temperature sensitive mutations ofadenovirus. Cold Spring Habor Symposia on Quantitative Biology,1974,39:439-446.
143. Hamer J. E., Farrall L., Orbach J., et al.. Host species-specific conservation of a family of repeatedDNA sequences in the genome of a fungal plant pathogen. Proc Natl Acad Sci USA,1989,86:9981-9985.
144. Han Y., Duan Y H, et al.. Genetic structure of three populations of Oxya chinensis in Shanxi, China.Zool Res.2002,23(1):76-80.
145. Harpending H. C., M. A. Batzer, et al.. Genetic traces of ancient demography. Proceedings of theNational Academy of Sciences.1998,95(4):1961-1967.
146. Hatira T., Saadet B., Hasan H. D., et al.. A multigene molecular phylogenetic assessment of truemorels (Morchella) in Turkey. Fungal Genetics and Biology,2010,47:672-682.
147. Hovm ller M. S.&Justesen, A. F.. Rates of evolution of avirulence phenotypes and DNA markersin a northwest European population of Puccinia striiformis f. sp. tritici. Molecular Ecology,2007,16,4637–4647.
148. Hovmoller M. S., Justesen A. F., Brown J. K. M.. Clonality and long-distance migration ofPuccinia striiformis in NW-Europe. Plant Pathol,2002,51:24-32.
149. Inuma T., Khodaparast S. A., Takamatsu S.. Multilocus phylogenetic analyses within Blumeriagraminis, a powdery mildew fungus of cereals. Molecular Phylogenetics and Evolution,2007,44,741-751.
150. Jevtic R., Pribakovic M., Stojanovic S., et al.. Screening the virulence of Erysiphe graminis DC.Ex Merat f. sp. tritici Em. Marchal in mobile nurseries. Plant Prot.1991,42:21-31.
151. Joseph S., Joshua A. S., Douglas M. R., et al.. Comprehensive polymorphism survey elucidatespopulation structure of S. cerevisiae. Nature,2009,458:342-345.
152. Kanazin V., Talbert H., See D., et al.. Discovery and assay of single-nucleotide polymorphisms inbarley (Hordeum vulgare). Plant Mol Biol,2002,48:529-537.
153. Karen H., Katherine F. L., Donald H. P.. Evolutionary relationships of the cup-fungus genus Pezizaand Pezizaceae inferred from multiple nuclear genes: RPB2, β-tubulin, and LSU rDNA. MolecularPhylogenetics and Evolution,2005,36:1-23.
154. Kimura M.. Evolutionary rate at the molecular level. Nature,1968,217:624-626.
155. Kimura M.. The neutral theory of molecular evolution. Cambridge University Press, London.1983.
156. Kinoshita A., Sasaki H., Nara K.. Phylogeny and diversity of Japanese truffles (Tuber spp.)inferred from sequences of four nuclear loci. Mycologia,2011, DOI:10.3852/10-138.
157. Koltin Y. and Kenneth R.. The role of the sexual stage in the over-summering of Erysiphe graminisDC. f. sp. hordei Marchal under semiarid conditions. Annals of Applied Biology,1970,65,263-268.
158. Kota R., Varshney R. K., Thiel T., et al.. Generation and comparison of EST-derived SSRs andSNPs in barley (Hordeum vulgare L.). Hereditas,2001,135:145-151.
159. Krutovsky K. V., Neale D. B.. Nucleotide diversity and linkage disequilibrium in cold-hardiness-and wood quality-related candidate genes in douglas fir. Genetics,2005,171(4):2029-2041.
160. Lander E. S.. The new genomics: global views of biology. Science,1996,274:536-539.
161. Leath S. and Murphy J. P., Virulence genes of the wheat powdery mildew fungus, Erysiphegraminis f. sp. tritici in North Carolina. Plant Dis.1985,69:905.
162. Leath S.. Wheat powdery mildew in the USA: Status of pathogen virulence and host resistance.Integrated Control of Cereal Mildews: Virulence Patterns and Their Change.1991,22-32.
163. Leila M.C.. Variability of the wheat powdery mildew pathogen Blumeria graminis f.sp. tritici inthe2003crop season. Fitopatologia Brasileira.2005,30(4):420-422.
164. Limpert E., Felsenstein F. G., and Andrivon D.. Analysis of virulence in populations of wheatpowdery mildew in Europe. J. Phytopathol.1987,120:1-8.
165. Mahuku G., Peters R. D., Plattff H. W.. Random amplication polymorphic DNA (RAPD) analysisof Phytophthora infestans isolates collection in Canada during1994-1996. Plant Pathology,2000,49:252-260
166. Majer D., Mithen R., Lewis B., et al.. The use of AFLP fingerprinting for the detection of geneticvariation in fungi. Mycological Research (United Kingdom),1996,100:1107-1111.
167. Marshall. Snipping away at genome patenting. Science,1997,277(19):1752-1753.
168. McDermott J. M., Brandle U., Dutly F., et al.. Genetic variation in powdery mildew of barley:Development of RAPD, SCAR and VNTR markers. Phytopathology.1994,84(11):1316-1321.
169. McDonald B. A. and Linde C.. Pathogen population genetics, evolutionary potential and durableresistance. Annu. Rev. Phytopathol.2002,40,349–379.
170. McDonald B. A. and Linde C.. The population genetics of plant pathogens and breeding strategiesfor durable resistance. Euphytica2002,124:163-180.
171. McDonald B. A. and McDermott J. M.. The population genetics of plant pathogenic fungi.BioScience1993,43:311-319.
172. McDonald B.A.. Population genetics of plant pathogenic fungi. Encyclopedia of Plant and Cropscience,2007,1046-1048.
173. McDonald B.A.. The population genetics of fungi: Tools and techniques. Phytopathology1997,87,448–453.
174. Michael R., Carrie S. T., Briana L. G., et al.. Genomic patterns of nucleotide diversity in divergentpopulation of U.S. weedy rice. BMC Evolutionary Biology,2010,10:180.
175. Namuco L. O., Coffman W. R., Bergstrom G. C., et al.. Virulence spectrum of the Erysiphegraminis f. sp. tritici population in New York. Plant Dis.1987,71:539-541.
176. Nei M.. Molecular Evolutionary Genetics. New York: Columbia University Press,1987,176-192.
177. Niewoehner A. S. and Leath S.. Virulence of Blumeria graminis f. sp. tritici on winter wheat in theeastern United States. Plant Dis.1998,82:64-68.
178. O’Donnell K., Ward T. J., Aberra D., et al.. Multilocus genotyping and molecular phylogeneticsresolve a novel head blight pathogen within the Fusarium graminearum species complex fromEthiopia. Fungal Genetics and Biology,2008,45:1514-1522.
179. O'Dell M., Wolfe M. S., Flavell R. B., et al.. Molecular variation in populations of Erysiphegraminis on barley, oats and rye. Plant Pathology.1989,38(3):340-351.
180. Okoli C. A. N., Carder J. H., Barbara D. J.. Restriction fragment length polymorphisms (RFLPs)and the relationships of some host-adapted isolats of Verticillium dahliae. Plant Pathology,1994,43:33-40
181. Olivieri I D Couvet, P H Gouyon. Trends Evolution,1990,5:207-210.
182. Pan Z, Yang X B, Pivonia S, et al.. Long-term predietion of soybean rust entry into the continentalUnited States. Plant Disease,2006,90:840-846.
183. Parks R., Carbone I., Murphy J. P., and Cowger C.. Population genetic analysis of an eastern U.S.wheat powdery mildew population reveals geographic subdivision and recent common ancestrywith U.K. and Israeli populations. Phytopathology,2009,99,840-849.
184. Parks R., Carbone I., Murphy J. P., Marshall D., and Cowger C.. Virulence structure of the easternU.S. wheat powdery mildew population. Plant Dis.2008,92:1074-1082.
185. Peakall R. and Smouse P.E.. GENALEX6: genetic analysis in Excel. Population genetic softwarefor teaching and research. Molecular Ecology Notes6,2006,288-295.
186. Persaud R. R., Lipps P. E.. Virulence genes and virulence gene frequencies of Blumeria graminisf.sp. tritici in Ohio. Plant Disease,1995,79:494-498.
187. Qu B., Li H. P., Zhang J. B., Xu Y. B., Huang T., Wu A. B., Zhao C. S., Carter J., Nicholson P. andLiao Y. C., Geographic distribution and genetic diversity of Fusarium graminearum and F.asiaticum on wheat spikes throughout China. Plant Pathology,2008,57:15-24.
188. Ramsay J. R., Multani D. S., Lyon B. R., RAPD-PCR identification of Verticillium dahliaeisolateswith differential pathogenicity on cotton. Aust J Agric Res,1996,47:681-693
189. Rashmi P., Amita C., Prija P., et al. Single nucleotide polymorphism in the genes of mce1andmce4operons of Mycobacterium tuberculosis: analysis of clinical isolates and tandard referencestrains. BMC Microbiology,2011,11:41.
190. Rosenberg N. A., and Nordborg M., Genealogical trees, coalescent theory and the analysis ofgenetic polymorphisms. Nat. Rev. Genet.2002,3:380-390.
191. Rosendahl S., Talor J. W., Development of multiple genetic markers for studies of genetic variationin arbuscular mycorrhiazl fungi using AFLP. Molecular Ecology,1997,(6):821-829.
192. Rousset F.1997. Genetic differentiation and estimation of gene flow from F-statistics underisolation by distance. Genetics,145:1219-1228.
193. Schaal B. A., Measurement of gene flow in Lupinus texensis. Nature,1980,284:450-451.
194. Shan W. X., Chen S.Y., Kang Z.S., et al. Genetic diversity in Puccinia striiformis f. sp triticirevealed by a pathogen genome-specific repetitive sequence. Canadian Journal of Botany,1998,76:587-595.
195. Slatkin M., Gene flow and the geographic structure of natural population. Science,1987,236:787-792.
196. Slovakova T., Svec M., and Miklovicova M., Do geographical barriers play any role in isolation ofpowdery mildew populations?. Biologia (Bratislava).2004,59:121-126.
197. Stephen B., Goodwin S., Clonal diversity and genetic differentiation of Phytophthora infestanspopulations in Northern and Central Mexico. Phytopathology,1992,82(9):955-961.
198. Tajima F. Statistical Method for Testing the Neutral Mutation Hypothesis by DNA Polymorphism.Genetics.1989,123(3):585-595.
199. Tamura, K., J. Dudley, et al. MEGA4: Molecular Evolutionary Genetics Analysis (MEGA)Software Version4.0. Molecular Biology and Evolution.2007,24(8):1596-1599.
200. Tavare S., Line-of-descent and genealogical processes and their applications in population geneticsmodels. Theor. Popul. Biol.1984,26:119-164
201. Templeton A. R., Nested clade analyses of phylogeographic data: Testing hypotheses about geneflow and population history. Mol. Ecol.1998,7:381-397.
202. Templeton A. R., Routman E., and Philips C. A., Separating population structure from populationhistory: A cladistic analysis of the geographical distribution of mitochondrial DNA haplotypes inthe tiger salamander, Ambystoma tigrinum. Genetics,1995,140:767-782.
203. Thorsten H., Lumbsch N., Wirtz R. L., et al. Higher level phylogenetic relationships ofeuascomycetes (Pezizomycotina) inferred from a combined analysis of nuclear and mitochondrialsequence data. Mycological Progress,2002,1(1):57-70.
204. Troch V., Audenaert K., Bekaert B., Hofte M. and Haesaert G., Phylogeography and virulencestructure of the powdery mildew population on its ‘new’ host triticale. BMC Evolutionary Biology,2012,12,76.
205. Vos P., Hogers R., Bleeker M., et al. AFLP: a new technique for DNA fingerprinting. Nucleic acidsresearch,1995,23:4407-4414.
206. Wang C.H., Li S.F., Genetic variability and relationships in mitochondrial DNA COⅡgenesequence of red common carps in China. Acta Genetica Sinica,2004,31(11):1226-1231.
207. Wang D.G., Fan J.B., Siao C., et al. Large-scale identification, mapping, and genotyping of singlenucleotide polymorphisms in the human genome. Science,1998,280:1077-1082.
208. Wang S.L., Sha Z.X., Tad S.S., et al. Quality assessment parameters for EST-derived SNPs fromcatfish. BMC Genomics,2008,9:45-50.
209. Welsh J. and McClelland M., Fingerprinting genomes using PCR with arbitraryprimers. Nucleic Acids Research,1990,18:7213-7218.181.
210. Whitlock M C, McCauley D E. Indirect measures of gene flow and migration: Fst1/(4Nm+1).Heredity,1999,82:117-125.
211. Williams J., Kubelik A., Livak K., et al. DNA polymorphisms amplified by arbitrary primers areuseful as genetic markers. Nucleic acids research,1990,18:6531-6535.
212. Wolfe M. S., Schwarzbach E., Patterns of race changes in powdery mildews. Ann Rev Phytopathol,1978,16:159-180.
213. Wolfe M. S., The use of virulence analysis in cereal mildews. Phytopathol Z,1975,82:297-307.
214. Wright S., Evolution in Mendelian populations. Genetics,1931,16:97-159.
215. Wright S., The genetical structure of population. Annual Eugenetics,1951,15:323-354.
216. Wyand R. A. and Brown J. K. M., Genetic and forma specialis diversity in Blumeria graminis ofcereals and its implications for host-pathogen co-evolution. Molecular Plant Pathology,2003,4(3),187-198.
217. Xiao M. G., Song F. J., Jiao J. F., Wang X. M., Xu H. X., Li H. J.. Identification of the gene Pm47on chromosome7BS conferring resistance to powdery mildew in the Chinese wheat landraceHongyanglazi. Theoretical and Applied Genetics,2013,126:1397-1403.
218. Yang J., Wang B., Li G., Bi Y.,&Yuan Z., Wheat stripe rust epidemic and virulence of Pucciniastriiformis f. sp tritici in China in2002. Plant Disease,2004,88,896–904.
219. Yeh F. C., Yang R. C., Boyle T. B. J., POPGENE, the user-friendly share are for population geneticanalysis. Molecular Biotechnology Center,1997,24:112-118.
220. Zabeau M., Vos P., Selective restriction fragment amplification: a general method for DNAfingerprinting. European patent application,1993,92:4026-4029.
221. Zeller K. A., Bowden R. L. and Leslie J. F., Population differentiation and recombination in wheatscab populations of Gibberella zeae from the United States. Molecular Ecology,2004,13:563-571.
222. Zeng S. M. And Luo Y., Long-distance spread and interregional epidemics of wheat stripe rust inChina. Plant Disease,2006,90,980–988.
223. Zhou H., Li D.Q., Zhang Y.G., et al. Study on mitochondrial DNA genetic diversity of TibetanAntelope. Genetic,2006,28(3):299-305.
224. Zietkiewicz E., Rafalski A., Labuda D., Genome fingerprinting by simple sequence repeat(SSR)-anchored polymerase chain reaction amplification. Genomics,1994,20:176-183.