拟南芥HSB1基因参与调控茉莉酸积累和植物抗病性的作用机制

理解植物抗病性的分子机制，是抗病育种和保障粮食安全的需要。在未发表的前期研究中，我们发现HSB1基因功能缺失导致植物对灰霉菌侵染和甜菜夜蛾幼虫取食的抗性降低；突变体对草酸抑制种子萌发、茉莉酸阻遏幼苗发育、茉莉酸诱导叶片衰老的敏感性均显著提高；hsb1突变在引起JA、JA-Ile、H2O2和NO等显著积累的同时可能下调乙烯的生物合成但不影响生长素抑制主根伸长反应。初步推测，HSB1参与调节茉莉酸合成、细胞氧化还原平衡以及植物的防御反应。在本申请项目中，我们将分析HSB1的表达特点及其对外源茉莉酸、H2O2、真菌侵染的响应能力，通过基因定点突变和转化截短片段等鉴定核心功能单元，定量乙烯及其合成前体的含量以及PDF1.2等抗病基因的表达，检测细胞氧化还原防护系统状态及相关基因的表达，分离HSB1的互作蛋白和共调控基因；明确HSB1在H2O2、NO和JA信号介导的植物防御反应中的作用及其分子机制。

Developing and planting disease-resistant varieties is one of the effective ways of combating crop losses caused by diseases and insects. Oriented towards the identification of key components and molecular mechanisms involved in plant defense responses against fungal infections, a focused genetic screening was carried out which led to the isolation of an Arabidopsis mutant, hsb1 (hyper-susceptible to botrytis 1) which shows more susceptible to infections by Botrytis cinerea as well as to attacks by herbivorous insect Spodoptera exigua than the wild type plants. But response to bacterial pathogen Pst DC3000 inoculations and inhibitory action of auxin on root elongation are not compromised by HSB1 mutations. HSB1 mutations cause increased sensitiveness to JA-inhibited seedling growth and JA-induced leaf senescence. Over-accumulations of jasmonates, H2O2 and NO and increased sensitivity of seed germination to supplied oxalic acid were also observed in hsb1 mutants. These results suggest the involvement of HSB1 in modulating cellular redox homeostasis, jasmonates accumulation and plant defense responses. To define the mechanisms of HSB1 functions, we propose to employ biochemical, transgenomic, genetic, and physiological approaches to: 1. study the expression pattern and subcellular location of HSB1 and its responsiveness to applied jasmonates, H2O2 and to fungal infections; 2. identify the interacting partners and co-regulated genes of HSB1; 3. observe whether the induced H2O2 and NO productions and calcium signaling by applied MeJA, H2O2 and fungal infections are altered by hsb1 mutations; 4. examine the possible impact on the biosynthesis of ethylene and its precursor ACC by hsb1 mutations and 5. to understand how HSB1 coordinates changes of cellular redox state and the interplay of JA, ethylene signaling pathways in response to biotic stresses.