Institute of Plant Biology, Biological Research Centre, Hungarian Academy of Sciences, 6726 Szeged, Hungary.
Doctoral School in Biology, Faculty of Science and Informatics, University of Szeged, 6720 Szeged, Hungary.
Int J Mol Sci. 2019 Jul 12;20(14):3432. doi: 10.3390/ijms20143432.
Seedling establishment following germination requires the fine tuning of plant hormone levels including that of auxin. Directional movement of auxin has a central role in the associated processes, among others, in hypocotyl hook development. Regulated auxin transport is ensured by several transporters (PINs, AUX1, ABCB) and their tight cooperation. Here we describe the regulatory role of the CRK5 protein kinase during hypocotyl hook formation/opening influencing auxin transport and the auxin-ethylene-GA hormonal crosstalk. It was found that the At mutant exhibits an impaired hypocotyl hook establishment phenotype resulting only in limited bending in the dark. The At mutant proved to be deficient in the maintenance of local auxin accumulation at the concave side of the hypocotyl hook as demonstrated by decreased fluorescence of the auxin sensor DR5::GFP. Abundance of the polar auxin transport (PAT) proteins PIN3, PIN7, and AUX1 were also decreased in the At hypocotyl hook. The AtCRK5 protein kinase was reported to regulate PIN2 protein activity by phosphorylation during the root gravitropic response. Here it is shown that AtCRK5 can also phosphorylate in vitro the hydrophilic loops of PIN3. We propose that AtCRK5 may regulate hypocotyl hook formation in through the phosphorylation of polar auxin transport (PAT) proteins, the fine tuning of auxin transport, and consequently the coordination of auxin-ethylene-GA levels.
种子萌发后需要精细调节植物激素水平,包括生长素。生长素的定向运动在相关过程中起着核心作用,例如在下胚轴钩发育中。生长素的调节运输是由几种转运蛋白(PINs、AUX1、ABCB)及其紧密合作来保证的。在这里,我们描述了 CRK5 蛋白激酶在下胚轴钩形成/张开过程中的调节作用,影响生长素运输和生长素-乙烯-GA 激素串扰。研究发现,At 突变体表现出下胚轴钩建立表型受损,仅在黑暗中有限弯曲。At 突变体被证明在维持下胚轴钩凹面局部生长素积累方面存在缺陷,如生长素传感器 DR5::GFP 的荧光减少所示。极性生长素运输(PAT)蛋白 PIN3、PIN7 和 AUX1 的丰度也在下胚轴钩中减少。AtCRK5 蛋白激酶被报道在根向重力反应中通过磷酸化调节 PIN2 蛋白活性。在这里,我们表明 AtCRK5 也可以在体外磷酸化 PIN3 的亲水环。我们提出 AtCRK5 可能通过磷酸化极性生长素运输(PAT)蛋白、精细调节生长素运输,从而协调生长素-乙烯-GA 水平,来调节下胚轴钩的形成。