Brassinazole represses tomato hypocotyl elongation via inhibition of cell division

Hypocotyl length is determined by cell division and elongation, which are associated with canonical cell cycle and endoreduplication. Plant hormone brassinosteroid (BR) is required for hypocotyl elongation under light while the roles of canonical cell cycle and endoreduplication in brassinosteroid-modulated hypocotyl elongation remain unclear. Here, we observed that brassinosteroid biosynthesis inhibitor brassinazole (BRZ) inhibited tomato hypocotyl elongation through inhibition of canonical cell cycle in the longitudinal direction, which was associated with the downregulation of cell cycle gene expression. Transcriptions of cell elongation gene SlRPEs were also repressed by BRZ during hypocotyl elongation which were positively correlated with the transcriptions of cell cycle genes. Analyses of cis-elements revealed that cyclin genes contained multiple E-box and BRRE motifs in the promoters, which were considered as BR-activated transcription factor BZR1 binding sites. Promoter activity assay using SlCYCU4;1 promoter-driven GUS revealed that BZR1 could activate SlCYCU4;1 transcription. We then analyzed nuclear DNA ploidy level and transcription of cell cycle genes in tomato cultivar ‘Micro-Tom’ which is a BR biosynthesis mutant showing dwarf morphology. Similar to the BRZ treatment, canonical cell cycle in the longitudinal direction was inhibited, and transcriptions of cell cycle genes and SlRPEs were repressed in ‘Micro-Tom’. Taken together, our results establish a connection between BR, canonical cell cycle and cell cycle genes, suggesting that inhibition of BR represses cell cycle genes to inhibit longitudinal cell division and consequent hypocotyl elongation.