Glycogen synthase kinase 3 (GSK3) kinases are evolutionarily conserved regulators of plant development and stress signaling, yet their contributions to thermotolerance in cool-adapted Brassica crops remain poorly understood. Here, we identified 16 BrSK genes in the Caixin (Brassica rapa ssp. chinensis var. parachinensis) genome, all harboring intact catalytic motifs indicative of functional kinase activity. Spatiotemporal expression profiling revealed preferential accumulation of BrSK transcripts in stem apices and floral organs during reproductive transition, while promoter analysis identified abundant heat- and abiotic stress-responsive cis-elements. Under heat stress, BrSK21, BrSK22, and BrSK23 displayed striking genotype-specific expression dynamics. BrSK21/22/23 transcripts were stably suppressed in the heat-tolerant cultivar '49-19' but transiently declined before rapidly rebounding in the heat-sensitive 'Liuye 50', mirroring RNA-seq profiles. Protein-protein interaction assays (Y2H, BiFC, and LCI) demonstrated specific associations between BrSK kinases and BrHSFA1. Functional validation via VIGS revealed that silencing of BrSK21 significantly enhanced thermotolerance, with triple silencing of BrSK21/22/23 conferring additive protection, indicating functional redundancy within the BrSK2 subfamily. Collectively, these findings establish the BrSK2 subfamily as negative regulators of heat tolerance in Caixin, likely via modulation of BrHSFA1 expression. This work identifies high-priority targets for molecular breeding of climate-resilient Brassica vegetables.
Haobo Yang, Kehang Chen, Rahat Sharif et al.· Plant Science· 0 citations
Sharing the most recent common ancestor, receptor-like kinases EXCESS MICROSPOROCYTES1 (EMS1) and BRASSINOSTEROID INSENSITIVE1 (BRI1) family members respectively perceive the peptide ligand TAPETUM DETERMINANT1 (TPD1) and the phytohormone brassinosteroids (BRs) to activate the same downstream BRI1 EMS SUPPRESSOR1 (BES1)/BRASSINAZOLE RESISTANT1 (BZR1) transcription factor family. Yet only their distinct canonical functions have been revealed. TPD1 specifically sustains tapetum development but is dispensable for global plant growth, whereas BRs regulate overall plant growth without impacting tapetum development. This generates a fundamental evolutionary conflict: gradual biochemical divergence with saltational biological diversification. Here, we identify an unrecognized redundant role of TPD1 and BR signaling in controlling early anther lobe formation. Simultaneous disruption of both pathways causes a lobeless anther defect, phenocopying the loss of the entire BES1/BZR1 family. Single-pathway disruption produces no such defect. Interestingly, we found that pathway specificity during tapetum development is caused by spatiotemporal ligand dynamics. The expression of DWF4 (encoding a rate-limiting BR biosynthetic enzyme) decreases sharply at the onset of tapetum development, while TPD1 expression remains stable. Consistently, exogenous BR application or the introduction of an active, ligand-independent BRI1 rescues tapetum defects in either the ems1 mutant or the dual-pathway-deficient mutant background. Our findings reconcile biochemical divergence and biological diversification with gradual evolution, likely stimulating study of the functional divergence of numerous other receptor-like kinases at multiple levels.
Weiyue Chen, Li-Ming He, Jingjie Zhang et al.· Current Biology· 0 citations
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