Plasma Membrane-Associated Ca2+-Binding Protein PCaP1 is Involved in Root Hydrotropism of Arabidopsis thaliana.
Plasma Membrane-Associated Ca2+-Binding Protein PCaP1 is Involved in Root Hydrotropism of Arabidopsis thaliana.
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DOI：
10.1093/pcp/pcz042
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发表时间：
2019-06
影响因子：
4.9
通讯作者：
Natsuki Tanaka-Takada;A. Kobayashi;Hideyuki Takahashi;Takehiro Kamiya;T. Kinoshita;M. Maeshima
中科院分区：
文献类型：
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作者：
Natsuki Tanaka-Takada;A. Kobayashi;Hideyuki Takahashi;Takehiro Kamiya;T. Kinoshita;M. Maeshima
根向水性是植物对水势梯度的重要生长反应。为了理解该机制，诸如 MIZU-KUSSEI 1 (MIZ1) 等基本元素已被广泛研究。我们研究了质膜相关阳离子结合蛋白 (PCaP1) 的生理作用，并检查了 PCaP1 功能丧失突变对根向水性的影响。尽管pcap1突变体的向地性是正常的，但pcap1敲除突变体在向水反应中表现出根部弯曲的缺陷。当 pcap1 幼苗用脱落酸（一种向地性负调节剂）处理时，幼苗表现出正常的向地性。通过引入带有内皮层特异性启动子的 PCaP1 基因组序列，明显挽救了 pcap1 突变体中的向水性缺陷。通过共聚焦激光扫描显微镜对表达 PCaP1 绿色荧光蛋白的根部进行分析表明，PCaP1 在大多数细胞中与质膜稳定相关，但在弯曲区域的内胚层细胞的细胞质中。此外，我们制备了在 pcap1 背景上过表达 MIZ1 的转基因系，发现 pcap1 向水性缺陷得到了挽救。我们的结果表明根伸长区内胚层细胞中的 PCaP1 参与了水溶反应。我们认为 PCaP1 通过独立于 MIZ1 的途径或作为将水势信号转导至 MIZ1 的上游组件之一来促进向水性。
Root hydrotropism is an essential growth response to water potential gradients in plants. To understand the mechanism, fundamental elements such as MIZU-KUSSEI 1 (MIZ1) have been investigated extensively. We investigated the physiological role of a plasma membrane-associated cation-binding protein (PCaP1) and examined the effect of PCaP1 loss-of-function mutations on root hydrotropism. pcap1 knockout mutants showed a defect in root bending as a hydrotropic response, although gravitropism was normal in pcap1 mutants. When pcap1 seedlings were treated with abscisic acid, a negative regulator of gravitropism, the seedlings showed normal gravitropism. The hydrotropism defect in pcap1 mutants was clearly rescued by introducing the genomic sequence of PCaP1 with an endodermis-specific promoter. Analysis of PCaP1-greenfluorescent protein-expressing roots by confocal laser scanning microscopy revealed that PCaP1 was stably associated with the plasma membrane in most cells, but in the cytoplasm of endodermal cells at the bending region. Furthermore, we prepared a transgenic line overexpressing MIZ1 on the pcap1 background and found that the pcap1 hydrotropism defect was rescued. Our results indicate that PCaP1 in the endodermal cells of the root elongation zone is involved in the hydrotropic response. We suggest that PCaP1 contributes to hydrotropism through a MIZ1-independent pathway or as one of the upstream components that transduce water potential signals to MIZ1.