Auxin represses stomatal development in dark-grown seedlings via Aux/IAA proteins
Auxin represses stomatal development in dark-grown seedlings via Aux/IAA proteins
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DOI：
10.1242/dev.109181
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发表时间：
2014-08-01
期刊：
影响因子：
4.6
通讯作者：
Hoecker, Ute
中科院分区：
文献类型：
--
作者：
Balcerowicz, Martin;Ranjan, Aashish;Hoecker, Ute
气孔的发育是通过内部和外部因素，是由一个复杂的信号网络集成严格调节。光是强烈促进气孔形成的外部因素。在这里，我们表明，生长素抗性aux/iaa突变体，如axr 3 -1，表现出去抑制气孔分化在黑暗中生长的幼苗。与野生型相比，在黑暗生长的axr 3 -1突变体中较高的气孔指数是由于气孔谱系中细胞分裂的增加。在生长素生物合成或生长素感知缺陷的突变体和用极性生长素运输抑制剂NPA处理的幼苗中，也观察到黑暗生长的幼苗中气孔过多。与这些研究结果相一致，外源生长素抑制气孔形成光生长的幼苗。综上所述，这些结果表明，生长素是一个负调节气孔发育在黑暗中生长的幼苗。上位性分析表明，axr 3 -1的行为在遗传上游的bHLH转录因子SPCH，MUTE和法马，以及YDA MAP激酶级联，但平行的阻遏物的光形态建成COP 1和受体样蛋白TMM。外源生长素的作用需要富含亮氨酸的重复受体样激酶的ER家族，这表明生长素至少部分地通过ER家族起作用。axr 3 -1在气孔谱系中的表达不足以改变气孔指数，这意味着细胞间通讯是介导生长素作用所必需的。总之，我们的研究结果表明，生长素信号有助于抑制气孔分化观察到在黑暗中生长的幼苗。
Stomatal development is tightly regulated through internal and external factors that are integrated by a complex signalling network. Light represents an external factor that strongly promotes stomata formation. Here, we show that auxin-resistant aux/iaa mutants, e.g. axr3-1, exhibit a de-repression of stomata differentiation in dark-grown seedlings. The higher stomatal index in dark-grown axr3-1 mutants when compared with the wild type is due to increased cell division in the stomatal lineage. Excessive stomata in dark-grown seedlings were also observed in mutants defective in auxin biosynthesis or auxin perception and in seedlings treated with the polar auxin transport inhibitor NPA. Consistent with these findings, exogenous auxin repressed stomata formation in light-grown seedlings. Taken together, these results indicate that auxin is a negative regulator of stomatal development in dark-grown seedlings. Epistasis analysis revealed that axr3-1 acts genetically upstream of the bHLH transcription factors SPCH, MUTE and FAMA, as well as the YDA MAP kinase cascade, but in parallel with the repressor of photomorphogenesis COP1 and the receptor-like protein TMM. The effect of exogenous auxin required the ER family of leucine-rich repeat receptor-like kinases, suggesting that auxin acts at least in part through the ER family. Expression of axr3-1 in the stomatal lineage was insufficient to alter the stomatal index, implying that cell-cell communication is necessary to mediate the effect of auxin. In summary, our results show that auxin signalling contributes to the suppression of stomatal differentiation observed in dark-grown seedlings.