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Summary Brassinosteroids (BRs) are a crucial class of plant hormones and regulate many important agronomic traits in crops. In Arabidopsis (Arabidopsis thaliana), BIR3 interacts with the BR receptor BRI1 and coreceptor BAK1 to negatively regulate BR signalling. In contrast, OsBIR3 interacts with OsBRI1 and OsBAK1 to positively regulate BR signalling in rice (Oryza sativa). However, our understanding of OsBIR3 remains incomplete. In this study, we isolated a reduced upper branch (rub1) mutant of rice, exhibiting a significant reduction in grain number. The causal gene for the mutant phenotype was LOC_Os04g41030 (OsBIR3). OsBIR3 interacts with both OsBRI1 and the remorin protein OsREM4.1, but interactions of the mutated Osbir3 with both OsBRI1 and OsREM4.1 were decreased. Furthermore, BL interferes with the interaction of OsBIR3 with OsBRI1, but promotes the interaction of OsBIR3 with OsREM4.1. Overexpression of OsREM4.1 and OsBRI1 individually in the rub1 mutant caused an exacerbation of the mutant phenotype. Additionally, OsBIR3 interacts with Brd2, involving BR biosynthesis in the early stage, and the interaction of the mutated brd2 with wild‐type OsBIR3 was increased. Besides, BL promotes the interaction between OsBIR3 and Brd2. Collectively, the data indicate that OsBIR3 plays a key role in maintaining the homeostasis of OsBRI1, OsREM4.1, and Brd2 at their respective protein levels. This work provides insight into the roles of OsBIR3 in BR signalling and biosynthesis pathways of rice.

Plant viruses drive widespread crop epidemics, yet the host plant responses across different cell types, particularly how these responses are influenced by cultivars with varying genetic backgrounds, including the presence of resistance (R) genes, remain poorly understood. Using tomato brown rugose fruit virus (ToBRFV) and two tomato cultivars, ‘Jinpeng No. 1’ (JP) and ‘Rutgers’ (RG), with different genetic backgrounds, this study used single‐cell RNA sequencing to explore infection dynamics and responses at the cellular level. Results showed that ToBRFV accumulated to different levels in the two cultivars, likely due to differences in their genetic backgrounds, particularly the distinct genotypes of the Tm‐22 and tm‐2 alleles. Following infection, the composition of cell types in tomato leaves also varied between the two cultivars. While the entry or movement of ToBRFV in the JP cultivar was not fully prevented early on, the viral accumulation in certain cell types of this cultivar was restricted. ToBRFV alters signalling pathways based on cell type and cultivars. Pseudotime analysis revealed that, in JP plants, ToBRFV reverses expression of brassinosteroid (BR) positive regulators during mesophyll cell development. Silencing positive BR regulators increased infection in JP plants, while suppressing it in RG plants, linking BR signalling to JP‐dependent resistance. Exogenous BR suppressed ToBRFV in JP but enhanced it in RG plants. This study reveals the differential involvement of BR signalling during viral infection in the two cultivars, offering a framework for future studies of plant‐virus interactions.

Leaf angle is a key factor in plant architecture and crop yield. Brassinosteroids (BRs) regulate many developmental processes, especially the leaf angle in monocots. However, the BR signalling pathway is complex and includes many unknown members. Here, we propose that Oryza sativa BRASSINOSTEROID-RESPONSIVE LEAF ANGLE REGULATOR 1 (OsBLR1) encodes a bHLH transcription factor, and positively regulates BR signalling to increase the leaf angle and grain length in rice (Oryza sativa L.). Lines overexpressing OsBLR1 (blr1-D and BLR1-OE-1/2/3) had similar traits, with increased leaf angle and grain length. Conversely, OsBLR1-knockout mutants (blr1-1/2/3) had erect leaves and shorter grains. Lamina joint inclination, coleoptile elongation, and root elongation assay results indicated that these overexpression lines were more sensitive to BR, while the knockout mutants were less sensitive. There was no significant difference in the endogenous BR contents of blr1-1/2 and wild-type plants. These results suggest that OsBLR1 is involved in BR signal transduction. The blr1-D mutant, with increased cell growth in the lamina joint and smaller leaf midrib, showed significant changes in gene expression related to the cell wall and leaf development compared with wild-type plants; furthermore, the cellulose and protopectin contents in blr1-D were reduced, which resulted in the increased leaf angle and bent leaves. As the potential downstream target gene of OsBLR1, the REGULATOR OF LEAF INCLINATION1 (OsRLI1) gene expression was up-regulated in OsBLR1-overexpression lines and down-regulated in OsBLR1-knockout mutants. Moreover, we screened OsRACK1A as an interaction protein of OsBLR1 using a yeast two-hybrid assay and glutathione-S-transferase pull-down.Key messageThe overexpression of OsBLR1 caused increased leaf angle and grain length, whereas OsBLR1-knockout mutants had the opposite phenotypes. OsBLR1 is a member in BR signalling pathway.

Brassinosteroid activity controls plant growth and development, often in a seemingly opposing or complex manner. Differential impact of the hormone and its signalling components, acting both as promoters and inhibitors of organ growth, is exemplified by meristem differentiation and cell expansion in above- and below-ground organs. Complex brassinosteroid-based control of stomata count and lateral root development has also been demonstrated. Here, mechanisms underlying these phenotypic outputs are examined. Among these, studies uncovering core brassinosteroid signalling components, which integrate with distinct peptide, hormone, and environmental pathways, are reviewed. Finally, the differential spatiotemporal context of brassinosteroid activity within the organ, as an important determinant of controlled growth, is discussed.

Metazoans and plants use pattern recognition receptors (PRRs) to sense conserved microbial-associated molecular patterns (MAMPs) in the extracellular environment. In plants, the bacterial MAMPs flagellin and elongation factor Tu (EF-Tu) activate distinct, phylogenetically related cell surface pattern recognition receptors of the leucine-rich repeat receptor kinase (LRR-RK) family called FLS2 and EF-Tu receptor, respectively. BAK1 is an LRR-RK coreceptor for both FLS2 and EF-Tu receptor. BAK1 is also a coreceptor for the plant brassinosteroid (BR) receptor, the LRR-RK BRI1. Binding of BR to BRI1 primarily promotes cell elongation. Here, we tune the BR pathway response to establish how plant cells can generate functionally different cellular outputs in response to MAMPs and pathogens. We demonstrate that BR can act antagonistically or synergistically with responses to MAMPs. We further show that the synergistic activities of BRs on MAMP responses require BAK1. Our results highlight the importance of plant steroid homeostasis as a critical step in the establishment of plant immunity. We propose that tradeoffs associated with plasticity in the face of infection are layered atop plant steroid developmental programs.

Susceptibility to the root-knot nematode Meloidogyne incognita in plants is thought to be a complex trait based on multiple genes involved in cell differentiation, growth and defence. Previous genetic analyses of susceptibility to M. incognita have mainly focused on segregating dominant resistance genes in crops. It is not known if plants harbour significant genetic variation in susceptibility to M. incognita independent of dominant resistance. To study the genetic architecture of susceptibility to M. incognita, we analysed nematode reproduction on a highly diverse set of 340 natural inbred lines of Arabidopsis thaliana with genome-wide association mapping. We observed a surprisingly large variation in nematode reproduction among these lines. Genome-wide association mapping revealed four quantitative trait loci (QTLs) located on chromosomes 1 and 5 of A. thaliana significantly associated with reproductive success of M. incognita, none of which harbours typical resistance gene homologues. Mutant analysis of three genes located in two QTLs showed that the transcription factor BRASSINAZOLE RESISTANT1 and an F-box family protein may function as (co-)regulators of susceptibility to M. incognita in Arabidopsis. Our data suggest that breeding for loss-of-susceptibility, based on allelic variants critically involved in nematode feeding, could be used to make crops more resilient to root-knot nematodes.

Leaf architecture directly determines canopy structure, and thus, grain yield in crops. Leaf droopiness is an agronomic trait primarily affecting the cereal leaf architecture but the genetic basis and underlying molecular mechanism of this trait remain unclear. Here, we report that DROOPY LEAF1 (DPY1), an LRR receptor-like kinase, plays a crucial role in determining leaf droopiness by controlling the brassinosteroid (BR) signaling output in Setaria, an emerging model for Panicoideae grasses. Loss-of-function mutation in DPY1 led to malformation of vascular sclerenchyma and low lignin content in leaves, and thus, an extremely droopy leaf phenotype, consistent with its preferential expression in leaf vascular tissues. DPY1 interacts with and competes for SiBAK1 and as a result, causes a sequential reduction in SiBRI1–SiBAK1 interaction, SiBRI1 phosphorylation, and downstream BR signaling. Conversely, DPY1 accumulation and affinity of the DPY1–SiBAK1 interaction are enhanced under BR treatment, thus preventing SiBRI1 from overactivation. As such, those findings reveal a negative feedback mechanism that represses leaf droopiness by preventing an overresponse of early BR signaling to excess BRs. Notably, plants overexpressing DPY1 have more upright leaves, thicker stems, and bigger panicles, suggesting potential utilization for yield improvement. The maize ortholog of DPY1 rescues the droopy leaves in dpy1, suggesting its conserved function in Panicoideae. Together, our study provides insights into how BR signaling is scrutinized by DPY1 to ensure the upward leaf architecture.

Plants exhibit a high level of developmental plasticity and growth is responsive to multiple developmental and environmental cues. Hormones are small endogenous signalling molecules which are fundamental to this phenotypic plasticity. Post-translational modifications of proteins are a central feature of the signal transduction pathways that regulate gene transcription in response to hormones. Modifications that affect the function of transcriptional regulators may also serve as a mechanism to incorporate multiple signals, mediate cross-talk, and modulate specific responses. This review discusses recent research that suggests hormone-responsive transcription factors are subject to multiple modifications which imply an additional level of regulation conferred by enzymes that mediate specific modifications, such as phosphorylation, ubiquitination, SUMOylation, and S-nitrosylation. These modifications can affect protein stability, sub-cellular localization, interactions with co-repressors and activators, and DNA binding. The focus here is on direct cross-talk involving transcription factors downstream of auxin, brassinosteroid, and gibberellin signalling. However, many of the concepts discussed are more broadly relevant to questions of how plants can modify their growth by regulating subsets of genes in response to multiple cues.

Glycogen synthase kinase 3 (GSK3)-like kinases play important roles in brassinosteroid (BR), abscisic acid, and auxin signaling to regulate many aspects of plant development and stress responses. The Arabidopsis thaliana GSK3-like kinase BR-INSENSITIVE 2 (BIN2) acts as a key negative regulator in the BR signaling pathway, but the mechanisms regulating BIN2 function remain unclear. Here we report that the histone deacetylase HDA6 can interact with and deacetylate BIN2 to repress its kinase activity. The hda6 mutant showed a BR-repressed phenotype in the dark and was less sensitive to BR biosynthesis inhibitors. Genetic analysis indicated that HDA6 regulates BR signaling through BIN2. Furthermore, we identified K189 of BIN2 as an acetylated site, which can be deacetylated by HDA6 to influence BIN2 activity. Glucose can affect the acetylation level of BIN2 in plants, indicating a connection to cellular energy status. These findings provide significant insights into the regulation of GSK3-like kinases in plant growth and development.