A regulatory network involving calmodulin controls phytosulfokine peptide processing during drought-induced flower abscission.

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.