对小麦白粉病菌生理小种三个鉴别寄主的抗生基因分析

采用基因推导法分析了三个鉴别寄主的抗性基因：白免３号和肯贵阿１号含有Ｐｍ４ａ；小白冬麦的抗性受一对隐性基因的控制，其抗谱不同于所有供试单基因系的抗谱。     

小麦白粉病菌群体生理小种和毒性基因结构分析与评价

以１９９０～１９９３年从河南省不同地区采集的３６４个小麦白粉病菌菌株标样为例，应用传统的生理小种鉴定方法和根据与已知抗白粉基因的互作推测毒性基因频率的方法，研究了河南省小麦白粉病菌群体生理小种和毒性基因结构。结果发现白粉病菌群体中生理小种组成及其频率有较大变化，亚号、１０号、１１号和１５号小种的频率均呈下降趋势，而３１号小种的频率呈大幅度上升，至１９９３年已达２０．７５％，跃居各小种之首；对１号、１１号、１５号和３１号小种的毒性基因谱分析发现，不同小种群的小种间至少存在一个以上毒性基因的差异，同小种群的不同小种间则在毒性基因谱上没有显著差异；另外，同一小种不同菌株间的毒性基因谱仍不完全相同，说明小种致病异质性是普遍存在的。毒性基因结构分析表明，Ｖ２、Ｖ２＋６和Ｖ８等毒性基因的频率有较大变化。文中还讨论了两种方法的优缺点和今后工作中如何改进等问题。     

12个小麦品种(系)白粉病抗性的遗传分析

利用17个不同来源和毒力的白粉菌菌株对12个小麦品种(系)进行苗期抗性鉴定和抗病性遗传分析,同时利用Pm2和Pm8基因的特异分子标记检测了相应基因。供试的12个品种至少能够抗11个白粉菌菌株。用E09、E20和Bg2菌株接种F₂群体,抗感植株分离比例和适合性测验证明这12个品种对不同白粉菌菌株的抗性均受1对显性基因控制。抗谱分析和基因紧密连锁分子标记(Xcfd81)分析表明良星66很可能含有Pm2或其等位基因。ω-黑麦碱基因(1RS染色体)和Glu-B1基因(1BS染色体)特异分子标记分析结果证明,山农20和郑麦9962含有T1BL·1RS易位染色体,即可能携带Pm8基因。由于Pm8基因对大多数菌株表现感病,所以这2个品种除Pm8外,还具有其他抗病基因。偃展4110与天民668对参试菌株的反应型表现一致,其他材料对不同菌株的反应型表现不同。     

若干小麦抗白粉病品系的有效抗病基因的测定

采用具有不同毒性基因的白粉菌菌株进行苗期接种，通过与已知抗病基因材料抗谱的相似性比较，对１７个抗白粉病育种品系的有效抗病基因进行了分析，其中３个阿拉拉特小麦杂种后代品系、４个Ｖ．Ｐ．Ｍ系统的杂种后代品系及另外１个杂交组合的后代品系含主效抗病基因Ｐｍ２；４个具有Ｖ．Ｐ．Ｍ或Ｃ３９血缘的品系及另外１个品系含主效抗病基因Ｐｍ４ ｂ；１个品系含Ｐｍ２＋６；２个普通小麦－黑麦６Ｄ／６Ｒ代换系的抗谱相似，且不     

2013年黑龙江省小麦白粉菌毒力结构分析

2013年从黑龙江省小麦生产区分离纯化57个单袍子堆小麦白粉菌菌株,用犯份小麦白粉病菌鉴别寄主进行毒力测定。结果表明,黑龙江省不同来源小麦白粉病菌群体具有相同的毒力结构,毒性基因V7,V8,V17,V19,VT a,V3c,V3f,V3e,VSa和VI+2+9的毒性频率均达80%以上,为黑龙江省小麦白粉菌的主要毒性基因;而Pm18(Ic),Pm21,Pm2+6,Pm5+6,Pm2+MLD5个抗性基因(或基因组合)抗90%以上的菌株,为黑龙江省有效杭白粉病基因(或基因组合)。研究结果可为小麦白粉病的抗病育种及杭病品种合理布局等方面提供参考。     

小麦近等基因系与白粉病菌互作的生理指标研究

小麦品种百农3217感白粉病,它的一个近等基因系(Xbd/百农3217(BC7F6))含抗病基因xbd,具有抗白粉病功能。以这两个品系为试验材料,接种白粉菌,分析了0~6 d两个品系叶片中过氧化氢(H2O2)的含量和7种代谢酶的活性,这些代谢酶包括超氧化物歧化酶(SOD)、过氧化氢酶(CAT)、谷胱甘肽还原酶(GR)、谷胱甘肽过氧化物酶(GPX)、脱氢抗坏血酸还原酶(DHAR)、抗坏血酸过氧化物酶(APX)和谷胱甘肽转硫酶(GST)等。目的是探讨在白粉菌和小麦植物的互作过程中,感病、抗病植物生理指标之间的差异。试验结果表明:接种白粉病菌后,H2O2含量在感病品系中显著下降,在抗病品系中显著上升;在白粉菌侵染进程中,CAT酶活性,感病与抗病品系无明显差异;感病品系叶片内SOD、GR、GPX、APX和GST活性在接种后期显著上升,高于抗病品系;DHAR活性变化则无明显规律。在白粉病侵染小麦植株过程中,H2O2具有重要作用,多种代谢机制共同参与,各种酶的总体表现影响了H2O2含量的变化。     

已知抗白粉病基因的小麦品种（系）在贵州的抗性表现

用采自贵州省的39个小麦白粉病菌株分别对9个鉴别品种和20个已知抗性基因的品种进行毒性频率测定，并于1995年-1996年将这些品种（系）种在3个点上进行异地鉴定，结果表明。抗白粉病基因pm1、pm3b、pm4a、pm4b、pm5、pm5和pm1 2 9、pm4＋8在贵州已无效或失效；pm12、pm17、pm18、pm19、pm21、pm2 6、pm2 M1d、pm2＋6＋1、pm2 4、pm2十4＋6、pm2＋4b 8在贵州是有效的。pm2、pm6、pm7、pm11和pm2x＋4在室内测定毒性频率较高，但在田间成株期严重率较低。小白冬（XBD）在室内外测定均表现很好的抗性．其抗谱与已知基因不同。     

小麦白粉病菌对三唑酮的抗药性测定方法的研究

试验比较了叶段法、小株法、试管苗法、活动苗圃法测定小麦白粉菌对三唑酮药剂的灵敏度的差异，并建立了灵敏度基线，发现了抗药菌株，可供测定小麦白粉菌的抗药性参考。     

小麦白粉病菌对国外引入的披碱草属植物的侵染

对采自我国和由美,加,日,捷,斯,阿（阿富汗）和前苏联引入了１８人种的披碱草,用我国小麦白粉病１１个生理小种的混合菌种进行接种,有１５个接种成功,用１４份发病披碱草上产生的白粉病菌分别回接小麦,也全部回拉成功,说明国外的披碱草和我国的一株具同源性,都属于我国小麦白粉病的寄主范围,具中间寄主传播病菌的潜力,对国外披碱草在疆域接壤的邻国间传播新小种等问题进行了讨论。     

小麦品系抗小麦白粉病基因分子标记鉴定

利用与3个抗小麦白粉病基因(PmPS5A, PmPS5B, PmY39)连锁的微卫星标记对分别由波斯小麦PS5和（或）小伞山羊草Y39衍生的72个小麦抗病品系进行了抗白粉病基因鉴定。在24个由波斯小麦PS5和小伞山羊草Y39合成的双二倍体Am9衍生的品系中,有2个品系含有PmPS5A的标记,有19个品系含有PmPS5B的标记,有7个品系含有PmY39的标记,还有     

小麦白粉病抗源材料的有效抗病基因分析

采用携带有不同毒性基因的白粉菌菌株进行苗期接种，通过与已知抗病基因材料抗谱的相似性比较分析，对３０多个小麦抗白粉病材料的有效抗病基因进行了测定，其中１份抗源材料具Ｐｍ２＋６；７份具Ｐｍ４ａ；１０份具Ｐｍ４ｂ；２份具Ｐｍ５；４份与小白冬麦的抗性相同，小白冬麦含有一特定的抗病基因；另外有８份材料的抗谱异于所供试的所有已知基因系，从中可能鉴定出新的抗病类型     

Race Specific Powdery Mildew Resistance in 31 Northwest European Wheat Cultivars

Race specific powdery mildew resistance in 23 winter wheat cultivars, eight spring wheat cultivars, and 14 lines/cultivars possessing known powdery mildew resistance genes, has been studied by analyzing host/pathogen interactions. The cultivars were tested as intact seedlings, and as detached primary leaf segments on water agar; both methods revealed reproducible and concordant results. The 45 cultivars/lines were divided into 24 resistance spectra according to the patterns of reaction to the powdery mildew isolates used. Of the 31 cultivars investigated, eight did not possess any of the resistance genes detected, and the remaining 23 were divided in 16 resistance spectra. The race specific resistance of nine cultivars was conferred by the single resistance genes Pm2, Pm4b, Pm5/Ml-i: or Pm6, while the race specific resistance of 14 cultivars was conferred by 2, 3, 4 or 5 genes in combination.     

Identification of Wheat Powdery Mildew Resistance Genes by Analysing Host-Pathogen Interactions

Fifty-nine winter wheat cultivars and thirteen lines possessing known powdery mildew resistance genes were inoculated with eleven different isolates. By comparing their resistance patterns the responsible major resistance genes of the above-mentioned cultivars have been determined. The so-called “Blaukorn” resistance is conditioned by gent Pm4b. The resistance patterns of Ml-i and Pm5 being similar, the relationship between them has to be analysed by segregating populations.     

Inheritance of the Powdery Mildew Resistance Mlk in Wheat

The inheritance of the Mlk powdery mildew resistance originating from ‘Heine 2174.50’ was analyzed by crossing the Mlk resistant cultivar ‘Ralle’× cv. ‘Amor’ (highly susceptible) and vice versa and by observing the reactions of F₁- and F₂-plants after inoculation with two different Mlk avirulent powdery mildew isolates. In all cases, a 3 (resistant): I (susceptible) segregation was found in F₂. The reactions of the F₂plants against the two powdery mildew isolates were identical in each case. Therefore, it is supposed that one dominant resistant gene is responsible for the resistant reactions against these two isolates. These results support the earlier assumption of Heun and Fischbeck (1987b) that the whole Mlk resistance pattern is controlled by a single gene.     

Inheritance of the Powdery Mildew Resistance Gene Pm9 in Relation to Pm1 and Pm2 of Wheat

The inheritance of the powdery mildew resistance gene Pm9 originating from the hexaploid spring wheat cultivar ‘Normandie’ was analyzed in relation to Pm1 and Pm2. Two leaf segments of individual P_1?, P_2?, F_1? and F₂-plants of the cross ‘Normandie’ (Pm1, 2, 9) בFederation’ (no known Pm gene) were inoculated separately with two powdery mildew isolates. Using powdery mildew isolate No. 6 virulent for Pm1 and Pm2 but avirulent for Pm9, a 1 resistant (r): 3 susceptible (s) F₂-segregation was found for the Pm9 gene. Using powdery mildew isolate No. 3 virulent for Pm1 and Pm9 but avirulent for Pm2, a 3 (r): 1 (s) F₂-segregation was found for the Pm2 gene. Combining the data of both experiments (leaf segments of identical plants had been used), a 9 (sr): 3 (ss): 3 (rr): 1 (rs) segregation resulted for the F₂ of this cross: therefore, independent inheritance of the genes Pm2 and Pm9 can be concluded. Similarly, the cross ‘Mephisto’ (Pm1, 2, 9) בAmor’ (no known Pm gene) was analyzed. The Pm9 gene again showed a monogenically recessive inheritance, whereas Pm1 showed a monogenically intermediate segregation upon inoculation with powdery mildew isolate No. 9a virulent for Pm2 and Pm9 but avirulent for Pm1. Combining the single gene segregations, linkage between both genes was found among the progenies. A distance of 8.5 cM was calculated. Analyzing a set of spring wheat cultivars with seven defined powdery mildew isolates, the presence of Pm1, Pm2 and Pm9 in these lines was verified; in most cases, Pm1 occurred together with Pm9.     

利用表达分析和基因沉默方法研究硫代硫酸硫转移酶基因TaTST与小麦抗白粉病反应的关系

硫代硫酸硫转移酶参与植物体内的硫代谢、氰化物的清除以及活性氧的生成与清除,与植物抗病反应密切相关。小麦抗、感白粉病近等基因系材料在接种白粉菌后均诱导表达硫代硫酸硫转移酶基因TaTST,并在接种后0~48 h内呈现2次诱导峰值,分别与白粉菌初次接触识别和附着胞侵入、吸器形成时间相对应,也与2次氧突发时间对应。TaTST在感病材料上的诱导表达水平明显高于在抗病材料上,由此导致的活性氧过度清除可能是导致感病反应的原因之一。TaTST也参与抗病反应过程。利用病毒诱导的基因沉默技术(virus-induced gene silencing, VIGS)创造了TaTST基因沉默的抗病植株。尽管充分发病时间后沉默植株叶片上并未观察到肉眼可见的病斑,但侵染早期白粉菌成功侵入频率的增加和次级菌丝的有限伸长说明TaTST沉默植株抗病水平下降。TaTST沉默导致乳突致密度下降和H₂O₂在细胞内的扩散时间延迟。因此,TaTST可能通过调节活性氧的积累和扩散、乳突的形成等小麦-白粉菌互作早期的寄主细胞反应而参与小麦对白粉菌的抗侵入过程。     

小麦白粉病菌诱导的TaWRKY34基因的鉴定与分析

WRKY转录因子在植物抗病防卫反应中发挥重要作用。利用cDNA宏阵列(macroarray)和RT-PCR相结合的方法,从小麦全长cDNA文库的WRKY转录因子中筛选出一个应答小麦白粉病菌胁迫的TaWRKY34转录因子,该基因编码464个氨基酸。染色体定位分析表明,该转录因子位于小麦第一同源群染色体的短臂上,并且只在细胞核中表达。其蛋白序列与拟南芥、大麦和葡萄抗病相关WRKY转录因子的亲缘关系较近,与其中的3个WRKY基因具有相似的表达模式。TaWRKY34在Pm16/北京8377抗白粉病近等基因系中,对小麦白粉病菌、水杨酸和茉莉酸诱导的表达模式存在差异。TaWRKY34可能与小麦对白粉菌的抗性有关。     

Genes for Powdery Mildew Resistance in Cultivars of Spring Wheat

Twenty-three cultivars of spring wheat were inoculated with nineteen different powdery mildew isolates; their ruction patterns hive been compared with those of twenty-two cultivars/lines carrying identified powdery mildew resistance genes. Applying the gene-for-gene hypothesis, it is evident that three cultivars have none of the resistance genes used, seven others (including ‘Solo’) may carry Pm4b, only. The resistance pattern of ‘Selpek’ is identical to A/-1 resistant cultivars of winter wheat and may be explained by the presence of Pm5. The resistance pattern of Pm5 (Mt-i) cultivars is very different from a number of ‘Kolibri’-related cultivars of spring wheat. Since either all or nothing of that specific pattern has been transferred to all cross progenies of ‘Kolibri’, a single gene is assumed to oe responsible for it, preliminarily designated as Ml-k. The cultivar ‘Mephisto’ carries the ‘Normandie’ resistance (Pwl 2, 9). In five cultivars to spring wheat the combined effects of at least two of the above-mentioned sources have been found. Despite the fact that ‘Normandie’ and ‘Sappo’ are not closely related. ‘Sappo’ shows the complete ‘Normandie’ resistance pattern plus that of Pm4b. The same is true for ‘Planet’ and ‘Walter’.