The plant innate immunity response in stomatal guard cells invokes G-protein-dependent ion channel regulation.
The plant innate immunity response in stomatal guard cells invokes G-protein-dependent ion channel regulation.
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DOI:
10.1111/j.1365-313x.2008.03657.x
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发表时间:
2008-12
期刊:
影响因子:
--
通讯作者:
Assmann SM
中科院分区:
文献类型:
--
作者:
Zhang W;He SY;Assmann SM
Stomata in the epidermes of terrestrial plants are important for CO2 absorption and transpirational water loss, and are also potential entryways for pathogen infection. Stomatal opening and closure are controlled by distinct mechanisms. Arabidopsis stomata have been shown to close in response to bacteria and pathogen-associated molecular patterns (PAMPs) as part of PAMP-triggered immunity (PTI). Here we show that flg22, a PAMP derived from bacterial flagellin, also inhibits light-induced stomatal opening. Consistent with our observations on stomatal opening, flg22 inhibits the guard cell inward K+ channels (K+in currents) that mediate K+ uptake during stomatal opening. Similar to previously documented K+ current changes triggered by exogenous elevation of H2O2 and nitric oxide (NO), with prolonged duration of flg22 exposure the outward K+ channels (K+out currents) of guard cells are also inhibited. In null mutants of the flg22 receptor, FLS2, flg22 regulation of stomatal opening, K+ currents, and K+out currents is eliminated. flg22 also fails to elicit these responses in null mutants of the sole canonical G protein α subunit, GPA1. The bacterial toxin, coronatine, produced by several pathogenic strains of Pseudomonas syringae, reverses the inhibitory effects of flg22 on both K+in currents and stomatal opening, indicating interplay between plant and pathogen in the regulation of plant ion channels. Thus, PAMP-triggered stomatal response involves K+ channel regulation, and this regulation is dependent on signaling via cognate PAMP receptors and a heterotrimeric G-protein. These new findings provide insights into the largely elusive signaling process underlying PTI-associated guard cell responses.