MDP25, A Novel Calcium Regulatory Protein, Mediates Hypocotyl Cell Elongation by Destabilizing Cortical Microtubules in Arabidopsis
MDP25, A Novel Calcium Regulatory Protein, Mediates Hypocotyl Cell Elongation by Destabilizing Cortical Microtubules in Arabidopsis
复制标题
MDP25 是一种新型钙调节蛋白，通过破坏拟南芥皮质微管的稳定性来介导下胚轴细胞伸长
DOI：
10.1105/tpc.111.092684
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发表时间：
2011-12-01
期刊：
影响因子：
11.6
通讯作者：
Mao, Tonglin
中科院分区：
文献类型：
--
作者：
Li, Jiejie;Wang, Xianling;Mao, Tonglin
下胚轴伸长的调节对植物的生长具有重要意义。微管在下胚轴细胞伸长过程中起着至关重要的作用。然而，这一过程背后的分子机制还不是很清楚。在这项研究中，我们描述了一种新的拟南芥微管不稳定蛋白25(MDP25)，它是下胚轴细胞伸长的负调控因子。我们在体外发现MDP25直接与微管结合并破坏微管的稳定性，从而促进微管解聚。Mdp25突变株系的幼苗黄化下胚轴较长。此外，MDP25过表达导致下胚轴细胞显著缩短，表现为皮层微管不稳定和定位异常，这表明MDP25在下胚轴细胞伸长的负调控中起着关键作用。尽管MDP25在正常情况下定位于质膜，但细胞内钙水平的增加导致MDP25部分从质膜上解离并进入胞浆。细胞MDP25结合并破坏皮质微管的稳定性，导致其重定向，随后抑制下胚轴细胞的伸长。我们的结果表明，MDP25通过对细胞质钙水平的反应来调节下胚轴细胞的伸长，从而在皮质微管上发挥作用。
The regulation of hypocotyl elongation is important for plant growth. Microtubules play a crucial role during hypocotyl cell elongation. However, the molecular mechanism underlying this process is not well understood. In this study, we describe a novel Arabidopsis thaliana microtubule-destabilizing protein 25 (MDP25) as a negative regulator of hypocotyl cell elongation. We found that MDP25 directly bound to and destabilized microtubules to enhance microtubule depolymerization in vitro. The seedlings of mdp25 mutant Arabidopsis lines had longer etiolated hypocotyls. In addition, MDP25 overexpression resulted in significant overall shortening of hypocotyl cells, which exhibited destabilized cortical microtubules and abnormal cortical microtubule orientation, suggesting that MDP25 plays a crucial role in the negative regulation of hypocotyl cell elongation. Although MDP25 localized to the plasma membrane under normal conditions, increased calcium levels in cells caused MDP25 to partially dissociate from the plasma membrane and move into the cytosol. Cellular MDP25 bound to and destabilized cortical microtubules, resulting in their reorientation, and subsequently inhibited hypocotyl cell elongation. Our results suggest that MDP25 exerts its function on cortical microtubules by responding to cytoplasmic calcium levels to mediate hypocotyl cell elongation.