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番茄 Asc 位点的突变赋予其对真菌病原体番茄早疫病菌的抗性。

Mutations at the Asc locus of tomato confer resistance to the fungal pathogen Alternaria alternata f. sp. lycopersici.

机构信息

Department of Genetics, Institute for Molecular Biological Sciences (IMBW), BioCentrum Amsterdam, Vrije Universiteit, De Boelelaan 1087, 1081, HV Amsterdam, The Netherlands.

出版信息

Theor Appl Genet. 1996 May;92(7):898-904. doi: 10.1007/BF00221904.

DOI:10.1007/BF00221904
PMID:24166557
Abstract

The fungal pathogen Alternaria alternata f. sp. lycopersici produces host-selective AAL-toxins that cause Alternaria stem canker in tomato. Susceptibility to the disease is based on the relative sensitivity of the host to the AAL-toxins and is controlled by the Asc locus on chromosome 3L. Chemical mutagenesis was employed to study the genetic basis of sensitivity to AAL-toxins and susceptibility to fungal infection. Following the treatment of seeds of a susceptible line with ethyl methanesulphonate (EMS), resistant M2 mutants were obtained. Most plants with induced resistances showed toxin-sensitivity responses that were comparable to those of resistant control lines carrying the Asc locus. In addition, genetic analysis of the mutagenised plants indicated that the mutations occurred at the Asc locus. Furthermore, novel mutants were identified that were insensitive to the AAL-toxins at the seedling stage but toxin-sensitive and susceptible to fungal infection at mature stages. No AAL-toxin-insensitive insertion mutants were identified following a transposon mutagenesis procedure. Molecular mechanisms involved in host defence against A a. lycopersici are discussed.

摘要

真菌病原菌交链格孢Alternaria alternata f. sp. lycopersici 产生对寄主具有选择性的 AAL 毒素,引起番茄的交链格孢茎溃疡病。对该疾病的易感性基于寄主对 AAL 毒素的相对敏感性,由染色体 3L 上的 Asc 基因座控制。化学诱变被用于研究对 AAL 毒素的敏感性和对真菌感染的易感性的遗传基础。在用乙基甲磺酸(EMS)处理易感系种子后,获得了抗性 M2 突变体。大多数诱导抗性的植物表现出与携带 Asc 基因座的抗性对照系相当的毒素敏感性反应。此外,对诱变植物的遗传分析表明,突变发生在 Asc 基因座上。此外,还鉴定出了在幼苗阶段对 AAL 毒素不敏感但在成熟阶段对毒素敏感且易受真菌感染的新型突变体。在用转座子诱变程序后,未鉴定出 AAL 毒素不敏感的插入突变体。讨论了宿主防御交链格孢Alternaria alternata f. sp. lycopersici 的分子机制。

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