A Pyrazole Partially Induces Brassinosteroid-Related Gene Expression, Leading to Salt Stress Sensitivity

Abstract

Pyrazoles have a broad range of biological properties that make them potentially useful for treating tuberculosis, microbial/fungal infections, and inflammation. In this study, the pyrazole 1,3-diaryl-1H-pyrazol-5-yl)(aryl)methanone (DPAM-1) prepared via catalytic aminooxygenation increased the sensitivity of Arabidopsis to salinity stress. An RNA-seq transcriptome analysis revealed DPAM-1 increased the expression of fewer genes than the coronatine treatment that enhanced salinity stress sensitivity, suggestive of the selective mode of action of DPAM-1. The up-regulated genes included marker genes for brassinosteroid (BR) responses. The responsiveness of BR-related genes, such as CONSTITUTIVE PHOTOMORPHOGENIC DWARF, DWARF4, Small auxin-up RNA_Ac1, and for touch 4 (TCH4)/xyloglucan endotransglucosylase/hydrolase 22 (XTH22), was verified by treatments with brassinolide (BL) and brassinazole (BR biosynthesis inhibitor) and analyses involving the brassinosteroid insensitive 1–5 (bri1-5) mutant carrying a weak allele encoding BRASSINOSTEROID INSENSITIVE 1 receptor kinase under our growth conditions. Among the examined genes, the transcription of only TCH4 increased after the DPAM-1 treatment. Examinations of the bri1-5 mutant indicated that DPAM-1 did not significantly affect the sensitivity of bri1-5 plants to salinity stress, suggesting the increased salinity stress sensitivity following the DPAM-1 treatment was partly mediated by the BR signaling pathway. In the present study, the BL treatment differentially altered the salinity stress tolerance of the Columbia and Wassilewskija accessions. The contribution of BR signaling to salinity stress tolerance during the diversification of Arabidopsis accessions and the potential applicability of DPAM-1 for elucidating the interplay between BR and other phytohormones were assessed.