The Defense Metabolite, Allyl Glucosinolate, Modulates Arabidopsis thaliana Biomass Dependent upon the Endogenous Glucosinolate Pathway

被引:36
|
作者
Francisco, Marta [1 ,2 ]
Joseph, Bindu [1 ]
Caligagan, Hart [1 ]
Li, Baohua [1 ]
Corwin, Jason A. [1 ]
Lin, Catherine [1 ]
Kerwin, Rachel [1 ]
Burow, Meike [3 ]
Kliebenstein, Daniel J. [1 ,3 ]
机构
[1] Univ Calif Davis, Dept Plant Sci, Davis, CA 95616 USA
[2] Spanish Council Sci Res, Grp Genet Breeding & Biochem Brass, Dept Plant Genet, Mis Biol Galicia, Pontevedra, Spain
[3] Univ Copenhagen, Copenhagen Plant Sci Ctr, DynaMo Ctr Excellence, Frederiksberg, Denmark
来源
基金
美国食品与农业研究所; 美国国家科学基金会; 新加坡国家研究基金会;
关键词
Arabidopsis; allyl GSL; GSL-induced responses; plant growth; defense metabolism; INSECT RESISTANCE; INDUCED RESPONSES; PIERIS-BRASSICAE; ECOLOGICAL COSTS; BIOSYNTHESIS; GENE; IDENTIFICATION; MYROSINASE; NETWORK; PLANTS;
D O I
10.3389/fpls.2016.00774
中图分类号
Q94 [植物学];
学科分类号
071001 ;
摘要
Glucosinolates (GSLs) play an important role in plants as direct mediators of biotic and abiotic stress responses. Recent work is beginning to show that the GSLs can also inducing complex defense and growth networks. However, the physiological significance of these GSL-induced responses and the molecular mechanisms by which GSLs are sensed and/or modulate these responses are not understood. To identify these potential mechanisms within the plant and how they may relate to the endogenous GSLs, we tested the regulatory effect of exogenous allyl GSL application on growth and defense metabolism across sample of Arabidopsis thaliana accessions. We found that application of exogenous allyl GSL had the ability to initiate changes in plant biomass and accumulation of defense metabolites that genetically varied across accessions. This growth effect was related to the allyl GSL side-chain structure. Utilizing this natural variation and mutants in genes within the GSL pathway we could show that the link between allyl GSL and altered growth responses are dependent upon the function of known genes controlling the aliphatic GSL pathway.
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收藏
页数:14
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