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A dual role for cell plate‐associated PI4Kβ in endocytosis and phragmoplast dynamics during plant somatic cytokinesis

机译:细胞体相关的PI4Kβ在植物体细胞胞质分裂过程中在胞吞和原生质体动力学中的双重作用

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摘要

Plant cytokinesis involves membrane trafficking and cytoskeletal rearrangements. Here, we report that the phosphoinositide kinases PI4Kβ1 and PI4Kβ2 integrate these processes in ( ) roots. Cytokinetic defects of an double mutant are accompanied by defects in membrane trafficking. Specifically, we show that trafficking of the proteins KNOLLE and PIN2 at the cell plate, clathrin recruitment, and endocytosis is impaired in double mutants, accompanied by unfused vesicles at the nascent cell plate and around cell wall stubs. Interestingly, plants also display ectopic overstabilization of phragmoplast microtubules, which guide membrane trafficking at the cell plate. The overstabilization of phragmoplasts in the double mutant coincides with mislocalization of the microtubule‐associated protein 65‐3 (MAP65‐3), which cross‐links microtubules and is a downstream target for inhibition by the MAP kinase MPK4. Based on similar cytokinetic defects of the and mutants and genetic and physical interaction of PI4Kβ1 and MPK4, we propose that PI4Kβ and MPK4 influence localization and activity of MAP65‐3, respectively, acting synergistically to control phragmoplast dynamics.
机译:植物胞质分裂涉及膜运输和细胞骨架重排。在这里,我们报道磷酸肌醇激酶PI4Kβ1和PI4Kβ2将这些过程整合到()根中。双突变体的细胞动力学缺陷伴随着膜运输中的缺陷。具体来说,我们显示在双重突变体中,蛋白质KNOLLE和PIN2在细胞板的运输,网格蛋白募集和内吞作用受损,伴随着新生细胞板和细胞壁短管周围未融合的囊泡。有趣的是,植物还表现出芦苇微管的异位过度稳定,从而指导细胞板的膜运输。双突变体中的原生质膜过度稳定与微管相关蛋白65-3(MAP65-3)的定位错误相吻合,后者使微管交联,是MAP激酶MPK4抑制作用的下游靶标。基于和突变体相似的细胞动力学缺陷以及PI4Kβ1和MPK4的遗传和物理相互作用,我们建议PI4Kβ和MPK4分别影响MAP65-3的定位和活性,协同作用来控制原生质膜动力学。

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