College of Horticulture, Shenyang Agricultural University, Shenyang, Liaoning 110866, People's Republic of China.
Key Laboratory of Protected Horticulture of Ministry of Education, Shenyang, Liaoning Province, China.
Plant Physiol. 2021 Apr 23;185(4):1829-1846. doi: 10.1093/plphys/kiab026.
Abscission of plant organs is induced by developmental signals and diverse environmental stimuli and involves multiple regulatory networks, including biotic or abiotic stress-impaired auxin flux in the abscission zone (AZ). Depletion of auxin activates AZ ethylene (ETH) production and triggers acceleration of abscission, a process that requires hydrogen peroxide (H2O2). However, the interaction between these networks and the underlying mechanisms that control abscission are poorly understood. Here, we found that expression of tonoplast intrinsic proteins, which belong to the aquaporin (AQP) family in the AZ was important for tomato (Solanum lycopersicum) pedicel abscission. Liquid chromatography-tandem mass spectrometry and in situ hybridization revealed that SlTIP1;1 was most abundant and specifically present in the tomato pedicel AZ. SlTIP1;1 localized in the plasma membrane and tonoplast. Knockout of SlTIP1;1 resulted in delayed abscission, whereas overexpression of SlTIP1;1 accelerated abscission. Further analysis indicated that SlTIP1;1 mediated abscission via gating of cytoplasmic H2O2 concentrations and osmotic water permeability (Pf). Elevated cytoplasmic levels of H2O2 caused a suppressed auxin signal in the early abscission stage and enhanced ETH production during abscission. Furthermore, we found that increasing Pf was required to enhance the turgor pressure to supply the break force for AZ cell separation. Moreover, we observed that SlERF52 bound directly to the SlTIP1;1 promoter to regulate its expression, demonstrating a positive loop in which cytoplasmic H2O2 activates ETH production, which activates SlERF52. This, in turn, induces SlTIP1;1, which leads to elevated cytoplasmic H2O2 and water influx.
植物器官的脱落是由发育信号和多种环境刺激诱导的，涉及多个调节网络，包括生物或非生物胁迫损伤脱落区（AZ）中的生长素流。生长素的耗竭激活 AZ 乙烯（ETH）的产生，并引发脱落的加速，这一过程需要过氧化氢（H2O2）。然而，这些网络之间的相互作用以及控制脱落的潜在机制还知之甚少。在这里，我们发现质膜内在蛋白（属于水通道蛋白（AQP）家族）在 AZ 中的表达对于番茄（Solanum lycopersicum）花梗脱落很重要。液质联用和原位杂交显示 SlTIP1;1 在番茄花梗 AZ 中丰度最高且特异性表达。SlTIP1;1 定位于质膜和液泡膜。SlTIP1;1 的敲除导致脱落延迟，而过表达 SlTIP1;1 则加速了脱落。进一步分析表明，SlTIP1;1 通过细胞质 H2O2 浓度和渗透水通透性（Pf）的门控来介导脱落。细胞质中 H2O2 水平的升高导致早期脱落阶段生长素信号受到抑制，并增强了脱落过程中的 ETH 产生。此外，我们发现增加 Pf 是增强膨压以提供 AZ 细胞分离所需断裂力所必需的。此外，我们观察到 SlERF52 直接结合到 SlTIP1;1 启动子上调节其表达，这表明了一个正反馈环，其中细胞质 H2O2 激活 ETH 产生，从而激活 SlERF52。这反过来又诱导 SlTIP1;1 的表达，导致细胞质中 H2O2 和水的涌入增加。
