phot1/NPH3信号系统在黑暗（A）和光照（B）条件下对PIN2内膜循环两条支路间平衡的调控机制
近日，植物学领域国际学术期刊The Plant Cell在线刊登了中科院植物研究所研究人员的最新研究成果“The Signal Transducer NPH3 Integrates the Phototropin1 Photosensor with PIN2-Based Polar Auxin Transport in Arabidopsis Root Phototropism”，研究者在文章中揭示了植物感知光信号并调控生长素极性运输的机制。
向光素1（phototropin1，phot1）是一种极性地分布在细胞膜上的植物蓝光信号受体，NPH3是其关键的信号转导蛋白。它们介导了植物的正（负）向光性弯曲等多种重要的生理反应。PIN2是拟南芥根尖生长素极性运输的关键蛋白。然而，关于光信号对PIN2蛋白在内膜循环的调控方式以及对生长素极性运输的影响，尚缺乏直接证据。
中科院植物研究所林金星研究组和德国波恩大学František Baluška博士合作，通过分子细胞学的手段发现：不同的光照条件能调控PIN2蛋白进入2条不同的内膜运输支路，一是指向植物液泡的蛋白质降解支路，二是指向细胞质膜的“膜-泡”循环支路。phot1能接受蓝光信号，并通过信号传递蛋白NPH3来调控PIN2蛋白在这两条支路间的平衡。当根尖定位的phot1接收到蓝光信号后，NPH3依赖的信号支路被激活，并促使位于液泡样区室（VLC）中的PIN2进入“膜-泡”循环支路，于是PIN2的极性定位增强，生长素极性运输速率也显著提高。当根尖细胞处于黑暗条件时，NPH3依赖的信号支路被关闭，更多的PIN2被储存于液泡样区室中，相应的生长素运输速率也随之降低。该项研究中，他们还利用了非损伤微测技术，定量测定了phot1和NPH3在蓝光照射下对生长素极性运输的影响。
上述研究结果揭示了植物蓝光受体phot1及其信号转导蛋白NPH3是如何通过调控PIN2的细胞极性，来控制根尖的生长素极性运输，以及如何调控根尖负向光性生长的分子机制，填补了根尖负向光性生长机制研究的空白。
该研究得到了科技部、国家自然科学基金委员会、中科院和中国博士后科学基金的支持。（生物谷Bioon.com）
doi:10.1105/tpc.111.094284
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The Signal Transducer NPH3 Integrates the Phototropin1 Photosensor with PIN2-Based Polar Auxin Transport in Arabidopsis Root Phototropism
Yinglang Wana, Jan Jasikb,c,1, Li Wanga, Huaiqing Haoa, Dieter Volkmannb, Diedrik Menzelb, Stefano Mancusod, František Baluškab,e,1 and Jinxing Lina,1,2
Under blue light (BL) illumination, Arabidopsis thaliana roots grow away from the light source, showing a negative phototropic response. However, the mechanism of root phototropism is still unclear. Using a noninvasive microelectrode system, we showed that the BL sensor phototropin1 (phot1), the signal transducer NONPHOTOTROPIC HYPOCOTYL3 (NPH3), and the auxin efflux transporter PIN2 were essential for BL-induced auxin flux in the root apex transition zone. We also found that PIN2-green fluorescent protein (GFP) localized to vacuole-like compartments (VLCs) in dark-grown root epidermal and cortical cells, and phot1/NPH3 mediated a BL-initiated pathway that caused PIN2 redistribution to the plasma membrane. When dark-grown roots were exposed to brefeldin A (BFA), PIN2-GFP remained in VLCs in darkness, and BL caused PIN2-GFP disappearance from VLCs and induced PIN2-GFP-FM4-64 colocalization within enlarged compartments. In the nph3 mutant, both dark and BL BFA treatments caused the disappearance of PIN2-GFP from VLCs. However, in the phot1 mutant, PIN2-GFP remained within VLCs under both dark and BL BFA treatments, suggesting that phot1 and NPH3 play different roles in PIN2 localization. In conclusion, BL-induced root phototropism is based on the phot1/NPH3 signaling pathway, which stimulates the shootward auxin flux by modifying the subcellular targeting of PIN2 in the root apex transition zone.
