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首页> 外文期刊>Developmental cell >Iron-Dependent Callose Deposition Adjusts Root Meristem Maintenance to Phosphate Availability
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Iron-Dependent Callose Deposition Adjusts Root Meristem Maintenance to Phosphate Availability

机译:铁依赖性Call糖沉积可调节根系分生组织维持以提高磷酸盐利用率

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摘要

Plant root development is informed by numerous edaphic cues. Phosphate (Pi) availability impacts the root system architecture by adjusting meristem activity. However, the sensory mechanisms monitoring external Pi status are elusive. Two functionally interacting Arabidopsis genes, LPR1 (ferroxidase) and PDR2 (P5-type ATPase), are key players in root Pi sensing, which is modified by iron (Fe) availability. We show that the LPR1-PDR2 module facilitates, upon Pi limitation, cell-specific apoplastic Fe and callose deposition in the meristem and elongation zone of primary roots. Expression of cell-wall-targeted LPR1 determines the sites of Fe accumulation as well as callose production, which interferes with symplastic communication in the stem cell niche, as demonstrated by impaired SHORT-ROOT movement. Antagonistic interactions of Pi and Fe availability control primary root growth via meristem-specific callose formation, likely triggered by LPR1-dependent redox signaling. Our results link callose-regulated cell-to-cell signaling in root meristems to the perception of an abiotic cue.
机译:植物根系的发育受许多前卫线索的影响。磷酸盐(Pi)的可用性通过调整分生组织的活动影响根系统的体系结构。然而,监测外部Pi状态的感觉机制是难以捉摸的。 LPR1(铁氧化酶)和PDR2(P5型ATPase)是两个功能上相互作用的拟南芥基因,是根系Pi感测中的关键角色,其受铁(Fe)的利用而改变。我们显示,LPR1-PDR2模块促进了Pi的局限性,使细胞特异性质外生铁和Fe质沉积在初级根的分生组织和延伸区中。以细胞壁为靶标的LPR1的表达决定了Fe积累以及call质产生的位点,这会干扰干细胞生态位中的共生性交流,这通过受损的SHORT-ROOT运动得以证明。 Pi和Fe可用性的拮抗相互作用通过分生组织特异的ose质形成控制初级根生长,这可能是由LPR1依赖性氧化还原信号触发的。我们的研究结果将根分生组织中call调调节的细胞间信号与非生物信号的感知联系起来。

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