Laboratory of Cell Dynamics, Graduate School of Bioagricultural Sciences, Nagoya University, Nagoya, Japan.
Institute for Advanced Research, Nagoya University, Nagoya, Japan.
Plant Cell Physiol. 2019 Jun 1;60(6):1331-1341. doi: 10.1093/pcp/pcz042.
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.
根向水性是植物对水势梯度的一种基本生长响应。为了理解这一机制，人们广泛研究了诸如 MIZU-KUSSEI 1（MIZ1）等基本要素。我们研究了质膜相关阳离子结合蛋白（PCaP1）的生理作用，并检验了 PCaP1 功能丧失突变对根向水性的影响。尽管 pcap1 突变体的向重力性正常，但 pcap1 敲除突变体在根弯曲作为向水性反应时表现出缺陷。当 pcap1 幼苗用脱落酸（一种向重力性的负调节剂）处理时，幼苗表现出正常的向重力性。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 突变体的向水性缺陷。通过共焦激光扫描显微镜分析表达 GFP 的 PCaP1 的根发现，PCaP1 在大多数细胞中与质膜稳定结合，但在内皮层细胞的弯曲区域的细胞质中。此外，我们在 pcap1 背景下制备了过量表达 MIZ1 的转基因系，并发现 pcap1 的向水性缺陷得到了挽救。我们的结果表明，根伸长区的内皮层细胞中的 PCaP1 参与了向水性反应。我们推测，PCaP1 通过 MIZ1 独立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。
