Benzoxazinoid Metabolites Regulate Innate Immunity against Aphids and Fungi in Maize
Benzoxazinoid Metabolites Regulate Innate Immunity against Aphids and Fungi in Maize
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DOI：
10.1104/pp.111.180224
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发表时间：
2011-09-01
期刊：
影响因子：
7.4
通讯作者：
Ton, Jurriaan
中科院分区：
文献类型：
--
作者：
Ahmad, Shakoor;Veyrat, Nathalie;Ton, Jurriaan
苯并恶嗪类化合物（Benzoxazinoids，BXs），如2，4-二羟基-7-甲氧基-2H-1，4-苯并恶嗪-3（4 H）-酮（DIMBOA），是禾本科植物的次生代谢产物。BX生物合成的第一步是将吲哚-3-甘油磷酸转化为吲哚。在玉米（Zea mays）中，该反应由苯并恶嗪酶1（BX 1）或吲哚甘油磷酸裂解酶（IGL）催化。Bx 1基因受发育控制，主要负责BX的产生，而Ig 1基因是可诱导的应激信号，如创伤，草食动物，或茉莉酸酯。为了确定BX在防御蚜虫和真菌中的作用，我们在igl突变体背景下比较了Bxl野生型和bxl突变株系之间的基础抗性，从而防止IGL产生BX。与Bx 1野生型植株相比，BX缺陷的bx 1突变体植株允许禾谷缢管蚜更好地发育，并且对真菌Setosphaeria turtica的穿透抗性受到影响。在主要组织破坏之前的阶段，R. padi和S. turtica引起DIMBOA-葡萄糖苷、DIMBOA和2-羟基-4，7-二甲氧基-1，4-苯并恶嗪-3-酮-葡萄糖苷（HDMBOA-glc）的积累增加，这在质外体叶提取物中最明显。用防御诱导剂壳聚糖处理同样增强了DIMBOA和HDMBOA-葡萄糖的质外体积累，但抑制了BX 1下游控制BX生物合成的基因的转录。用BX前体吲哚和DIMBOA处理后也得到这种抑制，但用HDMBOA-葡萄糖没有得到这种抑制。此外，BX-缺陷BX 1突变株系沉积壳聚糖诱导的胼胝质比BX 1野生型株系少，而质外体浸润与DIMBOA，但没有HDMBOA-葡萄糖，模仿壳聚糖诱导的胼胝质。因此，丁布在玉米先天免疫中起防御调节信号的作用，除了其作为杀生物防御代谢物的充分表征的活性之外，丁布还起作用。
Benzoxazinoids (BXs), such as 2,4-dihydroxy-7-methoxy-2H-1,4-benzoxazin-3(4H)-one (DIMBOA), are secondary metabolites in grasses. The first step in BX biosynthesis converts indole-3-glycerol phosphate into indole. In maize (Zea mays), this reaction is catalyzed by either BENZOXAZINELESS1 (BX1) or INDOLE GLYCEROL PHOSPHATE LYASE (IGL). The Bx1 gene is under developmental control and is mainly responsible for BX production, whereas the Igl gene is inducible by stress signals, such as wounding, herbivory, or jasmonates. To determine the role of BXs in defense against aphids and fungi, we compared basal resistance between Bx1 wild-type and bx1 mutant lines in the igl mutant background, thereby preventing BX production from IGL. Compared to Bx1 wild-type plants, BX-deficient bx1 mutant plants allowed better development of the cereal aphid Rhopalosiphum padi, and were affected in penetration resistance against the fungus Setosphaeria turtica. At stages preceding major tissue disruption, R. padi and S. turtica elicited increased accumulation of DIMBOA-glucoside, DIMBOA, and 2-hydroxy-4,7-dimethoxy-1,4-benzoxazin-3-one-glucoside (HDMBOA-glc), which was most pronounced in apoplastic leaf extracts. Treatment with the defense elicitor chitosan similarly enhanced apoplastic accumulation of DIMBOA and HDMBOA-glc, but repressed transcription of genes controlling BX biosynthesis downstream of BX1. This repression was also obtained after treatment with the BX precursor indole and DIMBOA, but not with HDMBOA-glc. Furthermore, BX-deficient bx1 mutant lines deposited less chitosan-induced callose than Bx1 wild-type lines, whereas apoplast infiltration with DIMBOA, but not HDMBOA-glc, mimicked chitosan-induced callose. Hence, DIMBOA functions as a defense regulatory signal in maize innate immunity, which acts in addition to its well-characterized activity as a biocidal defense metabolite.