Perturbing phosphoinositide homeostasis oppositely affects vascular differentiation in Arabidopsis thaliana roots.

Perturbing phosphoinositide homeostasis oppositely affects vascular differentiation in Arabidopsis thaliana roots.
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DOI:
10.1242/dev.155788
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发表时间:
2017-10-01
期刊:
Development (Cambridge, England)
影响因子:
--
通讯作者:
Rodriguez-Villalon A
Rodriguez-Villalon A
中科院分区:
其他
文献类型:
--
作者:
Gujas B;Cruz TMD;Kastanaki E;Vermeer JEM;Munnik T;Rodriguez-Villalon A

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植物维管网络由特化的韧皮部和木质部组成,它们经历两种不同的形态发生发育程序成为运输功能单位。然而液泡破裂是原生木质部分化的决定性步骤,原生韧皮部分子从不形成大的中央液泡。在这里,我们表明,磷脂酰肌醇4,5-二磷酸[PtdIns(4,5)P2]稳态的遗传干扰重新布线细胞贩运向液泡在拟南芥根。因此,增强的磷酸肌醇介导的液泡生物发生与木质部细胞中的过早程序性细胞死亡(PCD)和次生细胞壁的加工相关。相比之下,原韧皮部细胞中的液泡融合事件触发大液泡的异常形成,阻止细胞清除和组织功能。用布雷菲德菌素A(BFA)处理去除质膜上的肌醇5′磷酸酶子叶血管模式2,增加了质膜上PtdIns(4,5)P2的含量,破坏了原韧皮部的连续性。相反,BFA的应用废除了木质部组织中的液泡融合事件,而不阻止PCD,这表明存在额外的PtdIns(4,5)P2依赖性细胞死亡机制。总之,我们的数据表明,需要紧密的PM磷酸肌醇稳态来调节细胞内运输,从而有助于反向调节血管分化。总结:PtdIns(4,5)P2和PtdIns 4P的最佳比例的干扰对维管分化具有相反的影响,这是由于液泡生物发生在其分化程序中的不同作用。
The plant vascular network consists of specialized phloem and xylem elements that undergo two distinct morphogenetic developmental programs to become transport-functional units. Whereas vacuolar rupture is a determinant step in protoxylem differentiation, protophloem elements never form a big central vacuole. Here, we show that a genetic disturbance of phosphatidylinositol 4,5-bis-phosphate [PtdIns(4,5)P2] homeostasis rewires cell trafficking towards the vacuole in Arabidopsis thaliana roots. Consequently, an enhanced phosphoinositide-mediated vacuolar biogenesis correlates with premature programmed cell death (PCD) and secondary cell wall elaboration in xylem cells. By contrast, vacuolar fusion events in protophloem cells trigger the abnormal formation of big vacuoles, preventing cell clearance and tissue functionality. Removal of the inositol 5′ phosphatase COTYLEDON VASCULAR PATTERN 2 from the plasma membrane (PM) by brefeldin A (BFA) treatment increases PtdIns(4,5)P2 content at the PM and disrupts protophloem continuity. Conversely, BFA application abolishes vacuolar fusion events in xylem tissue without preventing PCD, suggesting the existence of additional PtdIns(4,5)P2-dependent cell death mechanisms. Overall, our data indicate that tight PM phosphoinositide homeostasis is required to modulate intracellular trafficking contributing to oppositely regulate vascular differentiation. Summary: Disturbance of the optimal ratio of PtdIns(4,5)P2 and PtdIns4P has opposing effects on vascular differentiation due to the distinct role of vacuolar biogenesis in their differentiation programs.
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