Effects of straw and silicon soil amendments on some foliar and stem-base diseases in pot-grown winter wheat

Four foliar and two stem-base pathogens were inoculated onto wheat plants grown in different substrates in pot experiments. Soils from four different UK locations were each treated in three ways: (i) straw incorporated in the field at 10 t ha⁻¹ several months previously; (ii) silicon fertilization at 100 mg L⁻¹ during the experiment; and (iii) no amendments. A sand and vermiculite mix was used with and without silicon amendment. The silicon treatment increased plant silica concentrations in all experiments, but incorporating straw was not associated with raised plant silica concentrations. Blumeria graminis and Puccinia recondita were inoculated by shaking infected plants over the test plants, followed by suitable humid periods. The silicon treatment reduced powdery mildew ( B. graminis ) substantially in sand and vermiculite and in two of the soils, but there were no effects on the slight infection by brown rust ( P. recondita ). Phaeosphaeria nodorum and Mycosphaerella graminicola were inoculated as conidial suspensions. Leaf spot caused by P. nodorum was reduced in silicon-amended sand and vermiculite; soil was not tested. Symptoms of septoria leaf blotch caused by M. graminicola were reduced by silicon amendment in a severely infected sand and vermiculite experiment but not in soil or a slightly infected sand and vermiculite experiment. Oculimacula yallundae (eyespot) and Fusarium culmorum (brown foot rot) were inoculated as agar plugs on the stem base. Severity of O. yallundae was reduced by silicon amendment of two of the soils but not sand and vermiculite; brown foot rot symptoms caused by F. culmorum were unaffected by silicon amendment. The straw treatment reduced severity of powdery mildew but did not detectably affect the other pathogens. Both straw and silicon treatments appeared to increase plant resistance to all diseases only under high disease pressure.     

Biocontrol options for Cirsium arvense with indigenous fungal pathogens

As a first step in the development of a mycoherbicide for biological control of Cirsium arvense indigenous fungal pathogens that had been isolated from diseased hosts were tested both singly and in combination on potted plants under environmental conditions. Disease symptoms (necroses, chloroses and macerations) and parameters of growth and development were evaluated to determine the potential for weed control. During 1998, Phoma destructiva, Phoma hedericola, a Mycelia sterilia and Puccinia punctiformis were inoculated singly. With the exception of the obligate biotroph P. punctiformis (local infections), the single inoculations reduced the measured parameters. A combined inoculum of P. punctiformis and Ph. hedericola was less effective than Ph. hedericola alone. In 1999, Ph. hedericola, Ph. destructiva, Ph. nebulosa and the Mycelia sterila were applied both singly and as a combined inoculum. Of all the tested inocula, the mixture of four pathogens had the greatest potential for biocontrol, significantly reducing reproductive capacity of the plants. These results demonstrate the importance of taking advantage of synergisms in developing a mycoherbicide.     

小麦/小麦秆锈菌亲和性互作的组织病理学及超微结构研究

利用化学显微技术和生物电镜技术，系统地研究了小麦秆锈菌在感病寄主上发育过程的组织学及超微结构特征。结果表明：小麦秆锈菌的发育过程可分为几个明显的阶段：孢子萌发和芽管形成，附着胞的形成和气孔下囊的分化，初生侵染菌丝和次生侵染菌丝的形成和生长，吸器母细胞和吸器的形成，夏孢子床和夏孢子堆的产生。小麦秆锈菌菌丝沿着细胞壁生长和蔓延．菌丝顶端细胞原生质稠密，代谢旺盛；吸器母细胞形成在细胞壁周围，吸器产生在细胞里面，呈指状，吸器外同和细胞膜区域有吸器外问质的存在。小麦秆锈菌发育早期，小麦细胞一直保持正常；而在发育后期，小麦细胞发生了质壁分离，叶绿体片层受到破坏。     

An analysis of genes for resistance against Indian stem rust races in two bread wheat cultivars

Summary The genetic constitution of two bread wheat accessions from the International Spring Wheat Rust Nurseries (E 5883 and E 6032) has been studied for reaction to four Indian races of stem rust. Analysis of E 5883 has revealed that for each of the races 15C, 21 and 40 a single dominant gene operates for resistance. The dominant gene against race 15C was identified as Sr6. The dominant genes for resistance against races 21 and 40 were found to be different from the genes described so far. Resistance against race 122 is controlled by a single recessive gene producing characteristically a 2 type of reaction. This gene was identified as Sr8.The resistance of E 6032 against each of the races 15C, 21 and 40 is controlled by two genes, one dominant and one recessive, which act independently. Dominant genes effective against 15C, 21 and 40 were conclusively identified as Sr6, Sr5 and Sr9b, respectively. From the correlated behaviour against races 15C and 40 as well as from the phenotypes of the resistance reactions rhe same recessive gene, undescribed so far, operates against the two races. The second recessive gene operating against race 21 was also observed to be different from those so far designated. E 6032 was, however, found to be susceptible to races 122.The presence of Sr6 both in E 5883 and E 6032 against race 15C was further confirmed through F₂ and F₃ segregation data.     

小麦条锈病罹病叶片核酸水解酶活力的变化

小麦初生叶接种条锈菌后，亲和反应寄主叶片ＲＮａｓｅ活性，分别在潜育期和产孢期呈双峰型增长；不亲和反应叶片ＲＮａｓｅ活性在侵染初期高于健康对照，但低于亲和性反应，其后随着病程发展，近免疫反应叶片ＲＮａｓｅ活性与对照相同，而中度抗病反应叶片也呈双峰增长，峰高及峰延续时间不同于亲和性反应。条锈菌侵染对ＤＮａｓｅ活性影响较小，亲和反应叶片仅在产孢阶段ＤＮａｓｅ活性有所增强，中度抗病反应叶片在显症时活性增强。     

小麦条锈菌果胶酶基因PsPL1的克隆与功能分析

【目的】研究小麦条锈菌果胶酶基因PsPL1的功能,确定其在小麦条锈菌侵染过程中的作用,为揭示小麦与病原菌互作的分子机理奠定理论基础。【方法】利用RACE技术扩增PsPL1基因全长,通过qRT-PCR对PsPL1的表达特征进行分析,并在酵母系统中验证其编码蛋白信号肽的分泌功能,最后通过HIGS技术沉默PsPL1基因,确定其在条锈菌侵染小麦过程中的作用。【结果】克隆得到PsPL1基因全长,其ORF长471bp,编码157个氨基酸;经预测PsPL1蛋白包含一个果胶酶保守结构域,N端含有一段由21个氨基酸组成的信号肽序列;经酵母系统验证,确定PsPL1蛋白信号肽具有分泌功能;qRT-PCR分析发现,PsPL1在条锈菌侵染早期表达上调;利用HIGS技术沉默PsPL1基因后,条锈菌的产孢量没有发生明显变化。【结论】成功克隆了小麦条锈菌果胶酶基因PsPL1,明确了其分泌特性及表达特征。     

Genetic mapping,marker assisted selection and allelic relationships for the Pu6 gene conferring rust resistance in sunflower

Rust resistance in the sunflower line P386 is controlled by Pu₆, a gene which was reported to segregate independently from other rust resistant genes, such as R₄. The objectives of this work were to map Pu₆, to provide and validate molecular tools for its identification, and to determine the linkage relationship of Pu₆ and R₄. Genetic mapping of Pu₆ with six markers covered 24.8 cM of genetic distance on the lower end of linkage Group 13 of the sunflower consensus map. The marker most closely linked to Pu₆ was ORS316 at 2.5 cM in the distal position. ORS316 presented five alleles when was assayed with a representative set of resistant and susceptible lines. Allelism test between Pu₆ and R₄ indicated that both genes are linked at a genetic distance of 6.25 cM. This is the first confirmation based on an allelism test that at least two members of the R_adv/R₄/R₁₁/ R_13a/R_13b/Pu₆ cluster of genes are at different loci. A fine elucidation of the architecture of this complex locus will allow designing and constructing completely new genomic regions combining genes from different resistant sources and the elimination of the linkage drag around each resistant gene.     

中国小麦秆锈菌鉴别寄主品种Rulofen抗秆锈病基因的单体分析

普通小麦品种Rulofen是我国小麦杆锈菌的鉴別寄主。用中国春单体系列和对Rulofen无毒性的小麦秆锈菌的三个生理小种21C3、34、34C2对Rulofen进行了抗秆锈病基因的单体分析,并将Rulofen所含的抗秆锈病基因与国际上已命名的Sr基因进行了异同比较。结果表明;Rulofen在2D染色体上含有兼抗三个供试生理小种的抗病基因Sr6.其抗性效应为;-;1~ 或1X~=-x~- ,因环境条件的影响,Sr6的抗性反应型不稳定;在5D染色体上含有兼抗21C3、34和34C2三个生理小种的抗病基因Sr30,其抗性效应为2=、抗秆锈病基因Sr6和Sr30对我国的小麦秆锈菌小种34类群都具有进一步的区分作用。     

2003-2004年我国小麦叶锈菌致病类型苗期鉴定及毒性分析

为明确小麦叶锈菌的毒性基因谱,对2003-2004采自我国的117株小麦叶锈菌菌株进行了致病性鉴定及毒性基因分析。结果表明:2003-2004年,117株小麦叶锈菌被划分为104个致病类型,其中优势类型为PHSS、PHTT和FHSS,其出现频率分别为4.27%、3.42%和2.56%。毒性基因V2 a、V9、V24、V3 a、V19、V38、V39、V40、V41、V42、V43和V46的毒性频率<30%,其对应的抗性基因为有效抗病基因,特别是V38的毒性频率为0,其对应的抗性基因有很好的抗叶锈性。V1、V3 ka、V30、V18、V14 ab、V15、V20、V21、V23、V28、V29、V32、V33+34、V36、V44和V45的毒性频率都在30%~60%之间,表明其对应的抗叶锈基因尚有一定的利用价值;V2 c、V3、V16、V26、V11、V17、VB、V10、V14 a、V2 b、V3 bg、V14 b、V25、V33、V34和VT3的毒性频率都>60%,表明其对应的抗叶锈基因在2003-2004年生产上单独使用几乎没有利用价值。     

A test of supposed mutants for stem rust resistance in wheat

Summary Eight stem rust (Puccinia graminis tritici Eriks. and Henn.) resistant lines (designated TICENA lines) that had been selected by Veiga et al. (1981) following gamma radiation of BH-1146 wheat (Triticum aestivum L.) were studied. Six of the lines were resistant to race 15B-1 of stem rust and susceptible to race 56, and proved to carry the gene Sr7a. TICENA 4 carries two unidentified genes, each giving resistance to one of the two races. TICENA 10 carries Sr6, Sr7a and an unidentified gene giving resistance to race 56 but not 15B-1. The results raise doubts about the supposed origin of the lines as mutants.