Control of basal jasmonate signalling and defence through modulation of intracellular cation flux capacity
Control of basal jasmonate signalling and defence through modulation of intracellular cation flux capacity
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DOI：
10.1111/nph.14754
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发表时间：
2017-12-01
期刊：
影响因子：
9.4
通讯作者：
Farmer, Edward E.
中科院分区：
文献类型：
--
作者：
Lenglet, Aurore;Jaslan, Dawid;Farmer, Edward E.
未知的机制紧密调节未受损组织中伤口诱导防御介质茉莉酸（JA）的基础活性。然而，拟南芥液泡双孔通道1（TPC 1（D454 N））中的脂肪酸加氧上调2（fou 2）突变体在未受损叶片中显示出高JA途径活性。这种突变体被用来探索机制控制基础JA通路的调节。FOU 2被重新突变，以产生新的'OUF'抑制突变体。膜片钳被用来检查TPC 1阳离子通道的特点，在ouf抑制突变体和fou 2。利用钙离子（Ca ~（2+））成像技术研究了fou 2对细胞内Ca ~（2+）浓度的影响，回收了6个具有近野生型（WT）JA通路活性的基因内ouf抑制子和1个影响通道孔的突变体ouf 8。在低的管腔钙浓度下，ouf 8对fou 2几乎没有可检测的影响。然而，增加液泡Ca 2+浓度造成通道阻塞，选择性地阻止K+流向细胞质。未受伤的fou 2细胞内Ca 2+浓度被发现低于未受伤的WT，但他们以类似的方式增加在两种基因型后wounding.Basal JA途径的活动可以单独控制通过操纵内膜阳离子通量的能力。我们认为，内膜电位的变化影响JA通路的活性。
Unknown mechanisms tightly regulate the basal activity of the wound-inducible defence mediator jasmonate (JA) in undamaged tissues. However, the Arabidopsis fatty acid oxygenation upregulated2 (fou2) mutant in vacuolar two-pore channel 1 (TPC1(D454N)) displays high JA pathway activity in undamaged leaves. This mutant was used to explore mechanisms controlling basal JA pathway regulation.fou2 was re-mutated to generate novel 'ouf' suppressor mutants. Patch-clamping was used to examine TPC1 cation channel characteristics in the ouf suppressor mutants and in fou2. Calcium (Ca2+) imaging was used to study the effects fou2 on cytosolic Ca2+ concentrations.Six intragenic ouf suppressors with near wild-type (WT) JA pathway activity were recovered and one mutant, ouf8, affected the channel pore. At low luminal calcium concentrations, ouf8 had little detectable effect on fou2. However, increased vacuolar Ca2+ concentrations caused channel occlusion, selectively blocking K+ fluxes towards the cytoplasm. Cytosolic Ca2+ concentrations in unwounded fou2 were found to be lower than in the unwounded WT, but they increased in a similar manner in both genotypes following wounding.Basal JA pathway activity can be controlled solely by manipulating endomembrane cation flux capacities. We suggest that changes in endomembrane potential affect JA pathway activity.