土壤所施衛明團隊發現鐵毒害影響植物根發育的機理

近日，New Phytologist發表中國科學院南京土壤研究所施衛明團隊題為「Excess iron stress reduces root tip zone growth through nitric oxide‐mediated repression of potassium homeostasis in Arabidopsis」的研究論文，研究了鐵離子過量時對植物根產生毒害過程中NO信號的作用。

根尖組織被認為是主要的響應鐵毒害的區域，並且要比根的其他組織更敏感。但是其機制目前仍然不是很清晰。本研究中研究人員利用一氧化氮信號的相關突變體和藥理學手段研究了一氧化氮(NO)信號在擬南芥根中的快速鐵響應機制。

研究發現，根尖的快速鐵響應機制與鉀離子(K+) 在根中的滯留有關。NO在根尖的積累顯著比根的其他區域高的的多。NO在過量的鐵存在時參與了主根尖的生長抑制，其部分與NO‐通過SNO1/SOS4誘導的鉀離子流失導致的根尖區細胞死亡有關。研究還發現，乙烯可以拮抗過量的鐵離子抑制的根生長和鉀離子外流，從而部分控制根尖的NO水平。因此研究人員認為。過量都鐵離子減緩了根都生長時由於根尖區域的NO被誘導增加有關，這個過程中，NO‐可能通過SNO1/SOS4影響了根中都鉀離子穩態。

Figure 11. A proposed model for nitric oxide (NO)-mediated Arabidopsis thaliana primary root tip zone growth under iron (Fe) excess.NO levels in root tips are increased significantly above levels elsewhere in the root and are involved in the arrest of primary root tip zone growth under excess Fe. NO-mediated inhibition of root growth is, at least in part, related to NO-induced K+ loss via nonselective cation channels (NSCCs), and increased SNO1 (sensitive to nitric oxide 1)/SOS4 (salt overly sensitive 4) activity-mediated pyridoxal-50-phosphate (PLP) is further implicated in this process. NO also mediates K+ homeostasis by the negative regulation of K+ uptake. The significant K+ loss can result in the loss of cell turgor (and hence arrest root growth) and either programmed cell death (PCD) or necrosis in the root apex. Meanwhile, excess Fe also reduces cell viability, associated with reactive oxygen species (ROS) accumulation and NO-induced hormone imbalance and protein S-nitrosylation. ROS has also been reported to activate NSCCs, resulting in K+ loss from the cell. Furthermore, Fe-induced ethylene can partially antagonize the reduction in excess Fe-mediated primary root growth by the control of NO levels. GORK1, guard cell outward-rectifying K+ channel 1.

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