The transcription factor HIG1/MYB51 regulates indolic glucosinolate biosynthesis in Arabidopsis thaliana
The transcription factor HIG1/MYB51 regulates indolic glucosinolate biosynthesis in Arabidopsis thaliana
复制标题
DOI：
10.1111/j.1365-313x.2007.03099.x
复制
发表时间：
2007-06-01
期刊：
影响因子：
7.2
通讯作者：
Fluegge, Ulf-Ingo
中科院分区：
文献类型：
--
作者：
Gigolashvili, Tamara;Berger, Bettina;Fluegge, Ulf-Ingo
硫代葡萄糖苷是一类植物次生代谢产物，在植物防御中起着抗草食动物的作用。一个先前确定的拟南芥激活标记线，显示改变水平的次生代谢产物，在这里被证明是吲哚和脂肪族硫代葡萄糖苷的含量的影响。观察到的化学型是由R2 R3-MYB转录因子基因HIGH 1（高吲哚葡萄糖芥子酸1，也称为MYB 51）激活引起的。HIG 1/MYB 51显示激活吲哚芥子油苷生物合成基因的启动子，导致吲哚芥子油苷的积累增加。相应的功能丧失突变体hig 1 -1含有低水平的硫代葡萄糖苷。相关转录因子ATR 1/MYB 34的过表达，这以前被描述为吲哚类芥子油苷和吲哚-3-乙酸稳态的调节剂，在hig 1 -1突变体背景下导致突变体化学型的部分拯救沿着严重的高生长素生长表型。MYB 122的过表达，另一个紧密的同源物的HIG 1/MYB 51，并没有拯救hig 1 -1化学型，但引起高生长素表型和吲哚芥子油苷的水平增加的野生型。相反，HIGH 1/MYB 51的过表达导致吲哚芥子油苷的特异性积累，而不影响生长素代谢和植物形态。机械刺激，如触摸或创伤瞬时诱导的表达，但不是ATR 1/MYB 34，和HIG 1/MYB 51过表达减少昆虫植食性的双选择试验所揭示的通性鳞翅目草食动物，甜菜夜蛾。我们推测，HIG 1/MYB 51是吲哚芥子油苷生物合成的调节因子，也控制着对生物挑战的反应。
Glucosinolates are a class of plant secondary metabolites that serve as antiherbivore compounds in plant defence. A previously identified Arabidopsis thaliana activation-tagged line, displaying altered levels of secondary metabolites, was shown here to be affected in the content of indolic and aliphatic glucosinolates. The observed chemotype was caused by activation of the R2R3-MYB transcription factor gene HIG1 (HIGH INDOLIC GLUCOSINOLATE 1, also referred to as MYB51). HIG1/MYB51 was shown to activate promoters of indolic glucosinolate biosynthetic genes leading to increased accumulation of indolic glucosinolates. The corresponding loss-of-function mutant hig1-1 contained low levels of glucosinolates. Overexpression of the related transcription factor ATR1/MYB34, which had previously been described as a regulator of indolic glucosinolate and indole-3-acetic acid homeostasis, in the hig1-1 mutant background led to a partial rescue of the mutant chemotype along with a severe high-auxin growth phenotype. Overexpression of MYB122, another close homologue of HIG1/MYB51, did not rescue the hig1-1 chemotype, but caused a high-auxin phenotype and increased levels of indolic glucosinolates in the wild-type. By contrast, overexpression of HIG1/MYB51 resulted in the specific accumulation of indolic glucosinolates without affecting auxin metabolism and plant morphology. Mechanical stimuli such as touch or wounding transiently induced the expression of HIG1/MYB51 but not of ATR1/MYB34, and HIG1/MYB51 overexpression reduced insect herbivory as revealed by dual-choice assays with the generalist lepidopteran herbivore, Spodoptera exigua. We hypothesize that HIG1/MYB51 is a regulator of indolic glucosinolate biosynthesis that also controls responses to biotic challenges.