WAG2 represses apical hook opening downstream from gibberellin and PHYTOCHROME INTERACTING FACTOR 5

WAG2 represses apical hook opening downstream from gibberellin and PHYTOCHROME INTERACTING FACTOR 5
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DOI:
10.1242/dev.081240
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发表时间:
2012-11
期刊:
影响因子:
4.6
通讯作者:
B. Willige;Eri Ogiso-Tanaka;M. Zourelidou;C. Schwechheimer
B. Willige;Eri Ogiso-Tanaka;M. Zourelidou;C. Schwechheimer
中科院分区:
生物学2区
文献类型:
--
作者:
B. Willige;Eri Ogiso-Tanaka;M. Zourelidou;C. Schwechheimer

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当双子叶植物在萌发过程中穿透土壤时,通过形成顶端钩来保护其茎尖分生组织。根尖钩形成是一个动态的过程,可分为钩形成、维持和开放。先前已经确定,这些过程需要植物激素生长素的运输和信号传导,以及植物激素乙烯和赤霉素(GA)的生物合成和信号传导。在这里,我们确定了一个生长素-GA串扰的分子机制,证明生长素转运调节蛋白激酶WAG 2是一个重要的转录靶点,在顶端钩开放下游GA信号。我们进一步表明,WAG 2是直接激活的植物色素相互作用因子5(PIF 5),光不稳定的相互作用的DELLA抑制GA途径。我们发现,wag 2突变体受损的抑制在黑暗中生长的幼苗顶端钩开口,这种表型与GA调节的WAG 2表达在凹(内)侧的顶端钩。此外,wag 2突变体也在钩中WAG 2表达位点处的局部生长素最大值的维持或形成中受损。WAG 2是PIN生长素外排促进剂的调节剂,并且与先前的数据一致,我们表明这种激酶可以磷酸化所有PIN形成的(PIN)调节顶端钩开口的蛋白质的中央细胞内环。因此,我们建议,顶端钩开口控制的差异GA调节积累的WAG 2和随后的本地变化PIN介导的生长素运输。
When penetrating the soil during germination, dicotyledonous plants protect their shoot apical meristem through the formation of an apical hook. Apical hook formation is a dynamic process that can be subdivided into hook formation, maintenance and opening. It has previously been established that these processes require the transport and signaling of the phytohormone auxin, as well as the biosynthesis and signaling of the phytohormones ethylene and gibberellin (GA). Here, we identify a molecular mechanism for an auxin-GA crosstalk by demonstrating that the auxin transport-regulatory protein kinase WAG2 is a crucial transcription target during apical hook opening downstream from GA signaling. We further show that WAG2 is directly activated by PHYTOCHROME INTERACTING FACTOR 5 (PIF5), a light-labile interactor of the DELLA repressors of the GA pathway. We find that wag2 mutants are impaired in the repression of apical hook opening in dark-grown seedlings and that this phenotype correlates with GA-regulated WAG2 expression in the concave (inner) side of the apical hook. Furthermore, wag2 mutants are also impaired in the maintenance or formation of a local auxin maximum at the site of WAG2 expression in the hook. WAG2 is a regulator of PIN auxin efflux facilitators and, in line with previous data, we show that this kinase can phosphorylate the central intracellular loop of all PIN-FORMED (PIN) proteins regulating apical hook opening. We therefore propose that apical hook opening is controlled by the differential GA-regulated accumulation of WAG2 and subsequent local changes in PIN-mediated auxin transport.