背景回顾：PIN-FORMED (PIN)-mediated polar auxin transport is involved in key developmental processes in plants. 

提出问题：Various internal and external cues influence plant development via the modulation of intracellular PIN polarity and, thus, the direction of polar auxin transport, but the mechanisms underlying these processes remain largely unknown. 

主要研究：PIN proteins harbor a hydrophilic loop (HL) that has important regulatory functions; here, we used the HL as bait in protein pulldown screening for modulators of intracellular PIN trafficking in Arabidopsis thaliana. 

结果1-磷酸化蛋白激酶：CPK29, a Ca2+-dependent protein kinase, was identified and shown to phosphorylate specific target residues on the PIN-HL that were not phosphorylated by other kinases. 

结果2-功能突变和位点突变：Furthermore, loss of CPK29 or mutations of the phospho-target residues in PIN-HLs significantly compromised intracellular PIN trafficking and polarity, causing defects in PIN-mediated auxin redistribution and biological processes such as lateral root formation, root twisting, hypocotyl gravitropism, phyllotaxis, and reproductive development. 

结论：These findings indicate that CPK29 directly interprets Ca2+ signals from internal and external triggers, resulting in the modulation of PIN trafficking and auxin responses.

 摘 要 

PIN接到的极性生长素转运参与植物很多关键的发育进程。各种外部和内部信号会通过调节细胞内PINs的极性定位，决定生长素极性运输的方向，从而影响植物的发育，但潜在的分子调控机制还不清楚。PIN蛋白包含一个亲水环（hydrophilic loop，HL），具有重要的调控功能；本文中，作者利用PIN蛋白的HL作为bait进行蛋白pulldown，以鉴定拟南芥中胞内PIN转运的调节子。作者发现一个钙离子依赖性的蛋白激酶CPK29能够磷酸化PIN-HL上不能被其它激酶磷酸化的特定氨基酸残基。此外，CPK29功能缺失突变或是PIN-HLs上特定磷酸化位点的突变会显著降低胞内PIN的转运和极性，导致PIN介导的生长素再分布和一些生物进程的缺陷，包括侧侧根形成、根弯曲、下胚轴向重力性、叶序和生殖发育。本文的研究结果揭示了CPK29能够直接将由内源或外源信号诱导的钙离子信号，转化为对PIN转运和生长素响应的调节。