D6PK AGCVIII Kinases Are Required for Auxin Transport and Phototropic Hypocotyl Bending in Arabidopsis[C][W]
D6PK AGCVIII Kinases Are Required for Auxin Transport and Phototropic Hypocotyl Bending in Arabidopsis[C][W]
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DOI：
10.1105/tpc.113.111484
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发表时间：
2013-05
期刊：
影响因子：
11.6
通讯作者：
B. Willige;Siv Ahlers;M. Zourelidou;Inês C. R. Barbosa;Emilie Demarsy;Martine Trévisan;Philip A Davis;M. Roelfsema;R. Hangarter;C. Fankhauser;C. Schwechheimer
中科院分区：
文献类型：
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作者：
B. Willige;Siv Ahlers;M. Zourelidou;Inês C. R. Barbosa;Emilie Demarsy;Martine Trévisan;Philip A Davis;M. Roelfsema;R. Hangarter;C. Fankhauser;C. Schwechheimer
这项工作证明了D6PK AGC激酶和PIN生长素转运蛋白是光致下胚轴弯曲所必需的。这些结果表明，D6PK介导的PIN转运蛋白的磷酸化促进了生长素在下胚轴中的运输，以确保适当的光变性下胚轴弯曲。蓝光诱导下胚轴弯曲是一种重要的适应过程，有助于植物优化光照条件。在拟南芥中，光性下胚轴弯曲是由蓝光受体和蛋白激动素1(PHIt1)和PHY2启动的。趋光性反应也需要生长素的运输，在PIN形成(PIN)的生长素外排促进剂的突变体中被证明是部分受损的。我们先前描述了AGCVIII激酶的D6蛋白激酶(D6PK)亚家族，我们提出了直接调节PIN介导的生长素运输的亚家族。在这里，我们证明了光致下胚轴弯曲强烈依赖于D6PKs和PIN蛋白PIN3、PIN4和PIN7的活性。虽然早期的蓝光和光依赖的信号事件不受D6PKs丢失的影响，但我们发现在复杂性增加的D6PK突变体中PIN3磷酸化逐渐丧失，这在D6PK d6pkl1 d6pkl2 d6pkl3四重突变体中最为严重。伴随而来的是D6PK和Pin突变体下胚轴中的基瓣生长素运输减少。根据我们的数据，我们认为依赖于D6PK的PIN调节促进了生长素的运输，下胚轴中的生长素运输是光依赖的下胚轴弯曲的先决条件。
This work demonstrates that D6PK AGC kinases and PIN auxin transporters are required for phototropic hypocotyl bending. The findings suggest that D6PK-mediated phosphorylation of PIN transporters promotes auxin transport in the hypocotyl to ensure proper phototropic hypocotyl bending. Phototropic hypocotyl bending in response to blue light excitation is an important adaptive process that helps plants to optimize their exposure to light. In Arabidopsis thaliana, phototropic hypocotyl bending is initiated by the blue light receptors and protein kinases phototropin1 (phot1) and phot2. Phototropic responses also require auxin transport and were shown to be partially compromised in mutants of the PIN-FORMED (PIN) auxin efflux facilitators. We previously described the D6 PROTEIN KINASE (D6PK) subfamily of AGCVIII kinases, which we proposed to directly regulate PIN-mediated auxin transport. Here, we show that phototropic hypocotyl bending is strongly dependent on the activity of D6PKs and the PIN proteins PIN3, PIN4, and PIN7. While early blue light and phot-dependent signaling events are not affected by the loss of D6PKs, we detect a gradual loss of PIN3 phosphorylation in d6pk mutants of increasing complexity that is most severe in the d6pk d6pkl1 d6pkl2 d6pkl3 quadruple mutant. This is accompanied by a reduction of basipetal auxin transport in the hypocotyls of d6pk as well as in pin mutants. Based on our data, we propose that D6PK-dependent PIN regulation promotes auxin transport and that auxin transport in the hypocotyl is a prerequisite for phot1-dependent hypocotyl bending.