Browse
Submit Data
Databases
API
Help

Dataset Information

29 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Behavior and possible function of Arabidopsis BES1/BZR1 homolog 2 in brassinosteroid signaling.

ABSTRACT: Two key transcription factors (TFs) in brassinosteroid (BR) signaling BRASSINOSTEROID INSENSITIVE 1-EMS-SUPPRESSOR 1 (BES1) and BRASSINAZOLE RESISTANT 1 (BZR1), belong to a small family with four BES1/BZR1 homologs (BEH1-4). To date, in contrast to the wealth of knowledge regarding BES1 and BZR1, little is known about BEH1-4. Here, we show that BEH2 was expressed preferentially in the roots and leaf margins including serrations, which was quite different from another member BEH4, and that BRs downregulated BEH2 through a module containing GSK3-like kinases and BES1/BZR1 TFs, among which BES1, rather than BZR1, contributed to this process. In addition, BEH2 consistently existed in the nucleus, suggesting that its subcellular localization is not under BR-dependent nuclear-cytoplasmic shuttling control. Furthermore, gene ontology analysis on RNA-seq data indicated that BEH2 may be implicated in stress response and photosynthesis. These findings might assist in the future elucidation of the molecular mechanisms underlying BR signaling.

SUBMITTER: Otani Y

PROVIDER: S-EPMC9196799 | biostudies-literature |

REPOSITORIES: biostudies-literature

ACCESS DATA

Json Xml

Similar Datasets

Protein farnesylation negatively regulates brassinosteroid signaling via reducing BES1 stability in Arabidopsis thaliana.

Project description:Brassinosteroids (BRs) are a group of steroidal phytohormones, playing critical roles in almost all physiological aspects during the life span of a plant. In Arabidopsis, BRs are perceived at the cell surface, triggering a reversible phosphorylation-based signaling cascade that leads to the activation and nuclear accumulation of a family of transcription factors, represented by BES1 and BZR1. Protein farnesylation is a type of post-translational modification, functioning in many important cellular processes. Previous studies demonstrated a role of farnesylation in BR biosynthesis via regulating the endoplasmic reticulum localization of a key bassinolide (BL) biosynthetic enzyme BR6ox2. Whether such a process is also involved in BR signaling is not understood. Here, we demonstrate that protein farnesylation is involved in mediating BR signaling in Arabidopsis. A loss-of-function mutant of ENHANCED RESPONSE TO ABA 1 (ERA1), encoding a β subunit of the protein farnesyl transferase holoenzyme, can alter the BL sensitivity of bak1-4 from a reduced to a hypersensitive level. era1 can partially rescue the BR defective phenotype of a heterozygous mutant of bin2-1, a gain-of-function mutant of BIN2 which encodes a negative regulator in the BR signaling. Our genetic and biochemical analyses revealed that ERA1 plays a significant role in regulating the protein stability of BES1.

| S-EPMC8360029 | biostudies-literature

Expression profiles of four BES1/BZR1 homologous genes encoding bHLH transcription factors in Arabidopsis.

Project description:Arabidopsis bHLH-type transcription factors-BRASSINOSTEROID INSENSITIVE 1-EMS-SUPPRESSOR 1 (BES1) and BRASSINAZOLE RESISTANT 1 (BZR1)-play key roles in brassinosteroid (BR) signaling. By contrast, the functions of the other four BES1/BZR1 homologs (BEH1-4) remain unknown. Here, we describe the detailed expression profiles of the BES1/BZR1 family genes. Their expressions were distinct regarding growth-stage dependence and organ specificity but exhibited some overlaps as well. Furthermore, their mRNA levels mostly remained unchanged responding to seven non-BR phytohormones. However, BEH1 and BEH2 were downregulated by brassinolide, suggesting a close association with the BR function. Additionally, BEH4 was ubiquitously expressed throughout the life of the plant but displayed some expression preference. For instance, BEH4 expression was limited to guard cells and the adjacent pavement cells in the leaf epidermis and was induced during growth progression in very young seedlings, suggesting that BEH4 is specifically regulated in certain contexts, although it is almost constitutively controlled.

| S-EPMC7251199 | biostudies-literature

Darkness and gulliver2/phyB mutation decrease the abundance of phosphorylated BZR1 to activate brassinosteroid signaling in Arabidopsis.

Project description:Light is essential for plant survival; as such, plants flexibly adjust their growth and development to best harvest light energy. Brassinosteroids (BRs), plant growth-promoting steroid hormones, are essential for this plasticity of development. However, the precise mechanisms underlying BR-mediated growth under different light conditions remain largely unknown. Here, we show that darkness increases the activity of the BR-specific transcription factor, BZR1, by decreasing the phosphorylated (inactive) form of BZR1 in a proteasome-dependent manner. We observed that COP1, a dark-activated ubiquitin ligase, captures and degrades the inactive form of BZR1. In support of this, BZR1 is abundant in the cop1-4 mutant. The removal of phosphorylated BZR1 in darkness increases the ratio of dephosphorylated to phosphorylated forms of BZR1, thus increasing the chance of active homodimers forming between dephosphorylated BZR1 proteins. Furthermore, a transcriptome analysis revealed the identity of genes that are likely to contribute to the differential growth of hypocotyls in light conditions. Transgenic misexpression of three genes under the 35S promoter in light conditions resulted in elongated petioles and hypocotyls. Our results suggest that light conditions directly control BR signaling by modulating BZR1 stability, and consequently by establishing light-dependent patterns of hypocotyl growth in Arabidopsis.

| S-EPMC4282538 | biostudies-literature

Sugar inhibits brassinosteroid signaling by enhancing BIN2 phosphorylation of BZR1.

Project description:Sugar, light, and hormones are major signals regulating plant growth and development, however, the interactions among these signals are not fully understood at the molecular level. Recent studies showed that sugar promotes hypocotyl elongation by activating the brassinosteroid (BR) signaling pathway after shifting Arabidopsis seedlings from light to extended darkness. Here, we show that sugar inhibits BR signaling in Arabidopsis seedlings grown under light. BR induction of hypocotyl elongation in seedlings grown under light is inhibited by increasing concentration of sucrose. The sugar inhibition of BR response is correlated with decreased effect of BR on the dephosphorylation of BZR1, the master transcription factor of the BR signaling pathway. This sugar effect is independent of the sugar sensors Hexokinase 1 (HXK1) and Target of Rapamycin (TOR), but requires the GSK3-like kinase Brassinosteroid-Insensitive 2 (BIN2), which is stabilized by sugar. Our study uncovers an inhibitory effect of sugar on BR signaling in plants grown under light, in contrast to its promotive effect in the dark. Such light-dependent sugar-BR crosstalk apparently contributes to optimal growth responses to photosynthate availability according to light-dark conditions.

| S-EPMC8153450 | biostudies-literature

Arabidopsis heterotrimeric G protein ? subunit, AGB1, regulates brassinosteroid signalling independently of BZR1.

Project description:The Arabidopsis thaliana heterotrimeric G protein ? subunit, AGB1, is involved in both abscisic acid (ABA) signalling and brassinosteroid (BR) signalling, but it is unclear how AGB1 regulates these signalling pathways. A key transcription factor downstream of BR, BZR1, and its gain-of-function mutant, bzr1-1, were overexpressed in an AGB1-null mutant, agb1-1, to examine their effects on the BR hyposensitivity and the ABA hypersensitivity of agb1-1, and to examine whether AGB1 regulates the functions of BZR1. Because the amino acid sequence of AGB1 contains 17 putative modification motifs of glycogen synthase kinase 3/SHAGGY-like protein kinases (GSKs), which are known components of BR signalling, the interaction between AGB1 and one of the Arabidopsis GSKs, BIN2, was examined. Expression of bzr1-1 alleviated the effects of a BR biosynthesis inhibitor, brassinazole, in both the wild type and agb1-1, and overexpression of BZR1 alleviated the effects of ABA in both the wild type and agb1-1. AGB1 did not affect the phosphorylation state of BZR1 in vivo. AGB1 interacted with BIN2 in vitro, but did not affect the phosphorylation state of BIN2. The results suggest that AGB1 interacts with BIN2, but regulates the BR signalling in a BZR1-independent manner.

| S-EPMC3733146 | biostudies-literature

Arabidopsis MYB30 is a direct target of BES1 and cooperates with BES1 to regulate brassinosteroid-induced gene expression.

Project description:A paradox of plant hormone biology is how a single small molecule can affect a diverse array of growth and developmental processes. For instance, brassinosteroids (BRs) regulate cell elongation, vascular differentiation, senescence and stress responses. BRs signal through the BES1/BZR1 (bri1-Ethylmethane Sulphonate suppressor 1/brassinazole-resistant 1) family of transcription factors, which regulate hundreds of target genes involved in this pathway, yet little is known of this transcriptional network. Through microarray and chromatin immunoprecipitation (ChIP) experiments, we identified a direct target gene of BES1, AtMYB30, which encodes an MYB family transcription factor. AtMYB30 null mutants display decreased BR responses and enhance the dwarf phenotype of a weak allele of the BR receptor mutant bri1. Many BR-regulated genes have reduced expression and/or hormone-induction in AtMYB30 mutants, indicating that AtMYB30 functions to promote expression of a subset of BR target genes. AtMYB30 and BES1 bind to a conserved MYB-binding site and E-box sequences, respectively, in the promoters of genes that are regulated by both BRs and AtMYB30. Finally, AtMYB30 and BES1 interact with each other both in vitro and in vivo. These results demonstrate that BES1 and AtMYB30 function cooperatively to promote BR target gene expression. Our results therefore establish a new mechanism by which AtMYB30, a direct target of BES1, functions to amplify BR signaling by helping BES1 activate downstream target genes.

| S-EPMC2814797 | biostudies-literature

Arabidopsis G-Protein β Subunit AGB1 Interacts with BES1 to Regulate Brassinosteroid Signaling and Cell Elongation.

Project description:In Arabidopsis, brassinosteroids (BR) are major growth-promoting hormones, which integrate with the heterotrimeric guanine nucleotide-binding protein (G-protein) signals and cooperatively modulate cell division and elongation. However, the mechanisms of interaction between BR and G-protein are not well understood. Here, we show that the G-protein β subunit AGB1 directly interacts with the BR transcription factor BES1 in vitro and in vivo. An AGB1-null mutant, agb1-2, displays BR hyposensitivity and brassinazole (BRZ, BR biosynthesis inhibitor) hypersensitivity, which suggests that AGB1 positively mediates the BR signaling pathway. Moreover, we demonstrate that AGB1 synergistically regulates expression of BES1 target genes, including the BR biosynthesis genes CPD and DWF4 and the SAUR family genes required for promoting cell elongation. Further, Western blot analysis of BES1 phosphorylation states indicates that the interaction between AGB1 and BES1 alters the phosphorylation status of BES1 and increases the ratio of dephosphorylated to phosphorylated BES1, which leads to accumulation of dephosphorylated BES1 in the nucleus. Finally, AGB1 promotes BES1 binding to BR target genes and stimulates the transcriptional activity of BES1. Taken together, our results demonstrate that AGB1 positively regulates cell elongation by affecting the phosphorylation status and transcriptional activity of BES1.

| S-EPMC5767185 | biostudies-literature

GmBEHL1, a BES1/BZR1 family protein, negatively regulates soybean nodulation.

Project description:Brassinosteroids (BRs) play an essential role in plant growth, and BRI1-EMS suppressor 1 (BES1)/brassinazole-resistant 1 (BZR1) family transcription factors integrate a variety of plant signaling pathways. Despite the fact that BRs inhibit nodulation in leguminous plants, how BRs modulate rhizobia-host interactions and nodule morphogenesis is unknown. Here, we show that GmBEHL1, a soybean homolog of Arabidopsis BES1/BZR1 homolog 1 (BEH1), is an interacting partner of Nodule Number Control 1, a transcriptional repressor that mediates soybean nodulation. GmBEHL1 was highly expressed at the basal parts of emerging nodules, and its expression gradually expanded during nodule maturation. The overexpression and downregulation of GmBEHL1 inhibited and enhanced the number of nodules, respectively, in soybean. Intriguingly, alterations in GmBEHL1 expression repressed the expression of genes in the BR biosynthesis pathway, including homologs of Arabidopsis Constitutive Photomorphogenesis and Dwarf and Dwarf 4. We also detected an interaction between GmBEHL1 and GmBIN2, a putative BR-insensitive 2 (BIN2) homolog, in soybean. Moreover, BR treatment reduced the number, but increased the size, of soybean nodules. Our results reveal GmBEHL1 to be a potent gene that integrates BR signaling with nodulation signaling pathways to regulate symbiotic nodulation.

| S-EPMC5955893 | biostudies-literature

Isolation and Functional Characterization of Soybean BES1/BZR1&nbsp;Homolog&nbsp;3-Like&nbsp;1 (GmBEH3L1) Associated with Dehydration Sensitivity and Brassinosteroid Signaling in Arabidopsis&nbsp;thaliana.

Project description:Brassinosteroid (BR) is an important steroid hormone that regulates plant development, abscisic acid (ABA) signaling, and responses to abiotic stress. We previously demonstrated that BEH3 (BES1/BZR1 Homolog 3) of Arabidopsis&nbsp;thaliana regulates dehydration and ABA responses by mediating proline metabolism. Furthermore, BEH3 negatively regulates BR-mediated hypocotyl elongation in dark-grown seedlings. However, the roles of BEH3 ortholog genes in the osmotic stress response of plants have remained largely unknown. Here, GmBEH3L1 (Glycine max BEH3-Like 1), a soybean (G.&nbsp;max) ortholog of the BEH3 gene of A. thaliana, was isolated and functionally characterized. GmBEH3L1 is induced by ABA, dehydration, and drought conditions. The GmBEH3L1-overexpressing transgenic lines (GmBEH3L1-OE/beh3) with the beh3 mutant background have ABA- and dehydration-sensitive phenotypes during early seedling growth, implying that GmBEH3L1 is involved in both osmotic stress and ABA sensitivity as a negative regulator in A. thaliana. Consistent with these results, GmBEH3L1-OE/beh3 complemental lines exhibit decreased expression levels of ABA- or dehydration-inducible genes. Under darkness, GmBEH3L1-OE/beh3 complemental lines display a short hypocotyl length compared to the beh3 mutant, indicating that GmBEH3L1 is linked to BR signaling. Together, our data suggest that GmBEH3L1 participates negatively in ABA and dehydration responses through BR signaling.

| S-EPMC9573144 | biostudies-literature

MYBL2 is a substrate of GSK3-like kinase BIN2 and acts as a corepressor of BES1 in brassinosteroid signaling pathway in Arabidopsis.

Project description:Plant steroid hormones, brassinosteroids (BRs), play important roles in plants. BRs regulate the expression of several thousand genes, half of which are induced and the other half repressed by the hormone. BRs signal through plasma membrane-localized receptor kinase brassinosteroid-insensitive 1 (BRI1), BRI1-associated receptor kinase (BAK1), and several intermediates to regulate the protein levels, cellular localizations, and/or DNA binding of BRI1-EMS suppressor 1 (BES1)/brassinazole-resistant 1 (BZR1) family transcription factors. Although BES1 is known to interact with other transcription factors, histone-modifying enzymes, and transcription elongation factors to activate BR-induced genes, how BES1 mediates the BR-repressed gene expression is not known. Here, we show that BES1 interacts with myeloblastosis family transcription factor-like 2 (MYBL2), a transcription repressor, to down-regulate BR-repressed gene expression. The loss-of-function mybl2 mutant enhances the phenotype of a weak allele of bri1 and suppresses the constitutive BR-response phenotype of bes1-D. The results suggest that suppression of BR-repressed gene expression is required for optimal BR response. Moreover, MYBL2 is a substrate of glycogen synthase kinase 3 (GSK3)-like kinase brassinosteroid-insensitive 2 (BIN2), which has been well established as a negative regulator in the BR pathway by phosphorylating and inhibiting the functions of BES1/BZR1. Unlike BIN2 phosphorylation of BES1/BZR1 leading to protein degradation, BIN2 phosphorylation stabilizes MYBL2. Such dual role of phosphorylation has also been reported in WNT signaling pathway in which GSK3 phosphorylation destabilizes β-catenin and stabilizes Axin, a scaffolding protein facilitating the phosphorylation of β-catenin by GSK3. Our results thus establish the mechanisms for BR-repressed gene expression and the integration of BR signaling and BR transcriptional network.

| S-EPMC3523856 | biostudies-literature

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data