The polar auxin transport is required for proper plant growth and development. D6 PROTEIN KINASE (D6PK) is required for the phosphorylation of PIN‐FORMED (PIN) auxin efflux carriers to regulate auxin transport, while the regulation of D6PK stabilization is still poorly understood. Here, we found that Cytosolic ABA Receptor Kinases (CARKs) redundantly interact with D6PK, and the interactions are dependent on CARKs' kinase activities. Similarly, CARK3 also could interact with paralogs of D6PK, including D6PKL1, D6PKL2, and D6PKL3. The genetic analysis shows that D6PK acts the downstream of CARKs to regulate Arabidopsis growth, including hypocotyl, leaf area, vein formation, and the length of silique. Loss‐of‐function of CARK3 in overexpressing GFP‐D6PK plants leads to reduce the level of D6PK protein, thereby rescues plant growth. In addition, the cell‐free degradation assays indicate that D6PK is degraded through 26 S proteasome pathway, while the phosphorylation by CARK3 represses this process in cells. In summary, D6PK stabilization by the CARK family is required for auxin‐mediated plant growth and development.

中文翻译：

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胞质 ABA 受体激酶磷酸化 D6 蛋白激酶，使其稳定，从而促进拟南芥生长

植物的正常生长和发育需要极性生长素运输。 D6 蛋白激酶 (D6PK) 是 PIN 形成 (PIN) 生长素外排载体的磷酸化所必需的，以调节生长素运输，而 D6PK 稳定性的调节仍知之甚少。在这里，我们发现胞质 ABA 受体激酶 (CARK) 与 D6PK 存在冗余相互作用，并且这种相互作用依赖于 CARK 的激酶活性。同样，CARK3 还可以与 D6PK 的旁系同源物相互作用，包括 D6PKL1、D6PKL2 和 D6PKL3。遗传分析表明D6PK作用于CARKs下游，调节拟南芥生长，包括下胚轴、叶面积、叶脉形成和长角果的长度。功能丧失卡克3在过度表达中GFP-D6PK植物导致D6PK蛋白水平降低，从而挽救植物生长。此外，无细胞降解测定表明，D6PK 通过 26 S 蛋白酶体途径降解，而 CARK3 的磷酸化抑制了细胞中的这一过程。总之，CARK 家族对 D6PK 的稳定作用是生长素介导的植物生长和发育所必需的。