Wang Sai, Ge Siqi, Liu Xianfeng, Cheng Lina, Li Ruizhen, Liu Yang, Cai Yue, Meng Sida, Tan Changhua, Jiang Cai-Zhong, Qi Mingfang, Li Tianlai, Xu Tao
College of Horticulture, Shenyang Agricultural University, Shenyang 110866, China.
Key Laboratory of Protected Horticulture of Ministry of Education, Shenyang Agriculture University, Shenyang, 110866, China.
Plant Cell. 2024 Dec 23;37(1). doi: 10.1093/plcell/koaf013.
Drought stress substantially decreases crop yields by causing flowers and fruits to detach prematurely. However, the molecular mechanisms modulating organ abscission under drought stress remain unclear. Here, we show that expression of CALMODULIN2 (CaM2) is specifically and sharply increased in the pedicel abscission zone in response to drought and plays a positive role in drought-induced flower drop in tomato (Solanum lycopersicum). Due to partial functional redundancy with SlCaM6, we generated the Slcam2 Slcam6 double mutant, which showed minimal flower drop under drought. SlCaM2 and SlCaM6 interacted with the transcription factor signal responsive 3L (SlSR3L), with the 3 proteins operating in the same pathway, based on genetic data. We identified Protease inhibitor26 (SlPI26) as a target gene of SlSR3L by DNA affinity purification sequencing and transcriptome analysis. SlPI26 specifically inhibited the activity of the phytaspase SlPhyt2, hence preventing the generation of active phytosulfokine peptide and negatively regulating drought-induced flower drop. SlCaM2 and SlCaM6 enhanced the repression of SlPI26 expression by SlSR3L, promoting drought-induced flower drop. In addition, the nonphototropic hypocotyl3 (SlNPH3)-Cullin3 (SlCUL3) complex, which relies on auxin, interacted with SlSR3L to induce its degradation. However, under drought conditions, SlNPH3-SlCUL3 function is compromised due to lower auxin concentration. These results uncover a regulatory network that precisely controls floral drop in response to drought stress.
干旱胁迫通过导致花朵和果实过早脱落，大幅降低作物产量。然而，干旱胁迫下调节器官脱落的分子机制仍不清楚。在这里，我们表明钙调蛋白2（CaM2）的表达在干旱胁迫下，于番茄（Solanum lycopersicum）花梗脱落区特异性且急剧增加，并在干旱诱导的落花中起积极作用。由于与SlCaM6存在部分功能冗余，我们构建了Slcam2 Slcam6双突变体，该突变体在干旱条件下落花极少。基于遗传数据，SlCaM2和SlCaM6与转录因子信号响应3L（SlSR3L）相互作用，这三种蛋白在同一途径中发挥作用。通过DNA亲和纯化测序和转录组分析，我们确定蛋白酶抑制剂26（SlPI26）是SlSR3L的一个靶基因。SlPI26特异性抑制植物半胱天冬酶SlPhyt2的活性，从而阻止活性植物硫肽的产生，并对干旱诱导的落花起负调控作用。SlCaM2和SlCaM6增强了SlSR3L对SlPI26表达的抑制作用，促进干旱诱导的落花。此外，依赖生长素的非向光性下胚轴3（SlNPH3）-Cullin3（SlCUL3）复合物与SlSR3L相互作用以诱导其降解。然而，在干旱条件下，由于生长素浓度降低，SlNPH3-SlCUL3的功能受损。这些结果揭示了一个精确控制干旱胁迫下落花的调控网络。
