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Regulation of Three Key Kinases of Brassinosteroid Signaling Pathway.

ABSTRACT: Brassinosteroids (BRs) are important plant growth hormones that regulate a wide range of plant growth and developmental processes. The BR signals are perceived by two cell surface-localized receptor kinases, Brassinosteroid-Insensitive1 (BRI1) and BRI1-Associated receptor Kinase (BAK1), and reach the nucleus through two master transcription factors, bri1-EMS suppressor1 (BES1) and Brassinazole-resistant1 (BZR1). The intracellular transmission of the BR signals from BRI1/BAK1 to BES1/BZR1 is inhibited by a constitutively active kinase Brassinosteroid-Insensitive2 (BIN2) that phosphorylates and negatively regulates BES1/BZR1. Since their initial discoveries, further studies have revealed a plethora of biochemical and cellular mechanisms that regulate their protein abundance, subcellular localizations, and signaling activities. In this review, we provide a critical analysis of the current literature concerning activation, inactivation, and other regulatory mechanisms of three key kinases of the BR signaling cascade, BRI1, BAK1, and BIN2, and discuss some unresolved controversies and outstanding questions that require further investigation.

SUBMITTER: Mao J

PROVIDER: S-EPMC7352359 | biostudies-literature | 2020 Jun

REPOSITORIES: biostudies-literature

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Regulation of Three Key Kinases of Brassinosteroid Signaling Pathway.

Mao Juan J Li Jianming J

International journal of molecular sciences 20200618 12

Brassinosteroids (BRs) are important plant growth hormones that regulate a wide range of plant growth and developmental processes. The BR signals are perceived by two cell surface-localized receptor kinases, Brassinosteroid-Insensitive1 (BRI1) and BRI1-Associated receptor Kinase (BAK1), and reach the nucleus through two master transcription factors, bri1-EMS suppressor1 (BES1) and Brassinazole-resistant1 (BZR1). The intracellular transmission of the BR signals from BRI1/BAK1 to BES1/BZR1 is inhi ...[more]

PMID: 32570783

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Project description:Small increases in temperature result in enhanced elongation of the hypocotyl and petioles and hyponastic growth, in an adaptive response directed to the cooling of the leaves and to protect the shoot meristem from the warm soil. This response, collectively termed as thermomorphogenesis, relies on the faster reversion of phyB Pfr at warmer temperatures, which leads to enhanced activity of the basic-helix-loop-helix PHYTOCHROME INTERACTING FACTOR 4 (PIF4). PIF4 acts as a molecular hub integrating light and temperature cues with endogenous hormonal signaling, and drives thermoresponsive growth by directly activating auxin synthesis and signaling genes. Growth promotion by PIF4 depends on brassinosteroid (BR) signaling, as indicated by the impaired thermoresponse of BR-defective mutants and the partial restoration of pifq thermoresponsive defects by brassinolide (BL) application. Also, phyB limits thermomorphogenic elongation through negative regulation of the E3 ubiquitin ligase COP1 that triggers nuclear degradation of multiple photomorphogenesis-promoting factors acting antagonistically to PIF4. COP1 is indeed observed to accumulate in the nucleus in darkness, or in response to warm temperatures, with constitutive photomorphogenic cop1 mutants failing to respond to temperature. Here we explored the role of BR signaling on COP1 function, by growing cop1 seedlings on BL or the inhibitor brassinazole (BRZ), under different light and temperature regimes. We show that weak cop1 alleles exhibit a hyposensitive response to BL. Furthermore, while cop1-6 mutants display as described a wild-type response to temperature in continuous darkness, this response is abolished by BRZ. Application of this inhibitor likewise suppressed temperature-induced COP1 nuclear accumulation in N. benthamiana leaves. Overall these results demonstrate that cop1-6 is not a temperature-conditional allele, but this mutation allows for a partially active protein which unveils a pivotal role of active BR signaling in the control of COP1 activity.

Project description:BackgroundGlycogen Synthase Kinase 3/SHAGGY-like kinases (GSKs) are multifunctional non-receptor ser/thr kinases. Plant GSKs are involved in hormonal signaling networks and are required for growth, development, light as well as stress responses. So far, most studies have been carried out on Arabidopsis or on other eudicotyledon GSKs. Here, we evaluated the role of TaSK1 and TaSK2, two homolog wheat (Triticum aestivum) GSKs, in brassinosteroid signaling. We explored in addition the physiological effects of brassinosteroids on wheat growth and development.ResultsA bin2-1 like gain-of-function mutation has been inserted respectively in one of the homoeologous gene copies of TaSK1 (TaSK1-A.2-1) and in one of the homoeologous gene copies of TaSK2 (TaSK2-A.2-1). Arabidopsis plants were transformed with these mutated gene copies. Severe dwarf phenotypes were obtained closely resembling those of Arabidopsis bin2-1 lines and Arabidopsis BR-deficient or BR-signaling mutants. Expression of BR downstream genes, SAUR-AC1, CPD and BAS1 was deregulated in TaSK1.2-1 and TaSK2.2-1 transgenic lines. Severe dwarf lines were partially rescued by Bikinin beforehand shown to inhibit TaSK kinase activity. This rescue was accompanied with changes in BR downstream gene expression levels. Wheat embryos and seedlings were treated with compounds interfering with BR signaling or modifying BR levels to gain insight into the role of brassinosteroids in wheat development. Embryonic axis and scutellum differentiation were impaired, and seedling growth responses were affected when embryos were treated with Epibrassinolides, Propiconazole, and Bikinin.ConclusionsIn view of our findings, TaSKs are proposed to be involved in BR signaling and to be orthologous of Arabidopsis Clade II GSK3/SHAGGY-like kinases. Observed effects of Epibrassinolide, Propiconazole and Bikinin treatments on wheat embryos and seedlings indicate a role for BR signaling in embryonic patterning and seedling growth.

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Regulation of Three Key Kinases of Brassinosteroid Signaling Pathway.

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Regulation of Three Key Kinases of Brassinosteroid Signaling Pathway.

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