RESUMO
Plants are equipped with the capacity to respond to a large number of diverse signals, both internal ones and those emanating from the environment, that are critical to their survival and adaption as sessile organisms. These signals need to be integrated through highly structured intracellular networks to ensure coherent cellular responses, and in addition, spatiotemporal actions of hormones and peptides both orchestrate local cell differentiation and coordinate growth and physiology over long distances. Further, signal interactions and signaling outputs vary significantly with developmental context. This review discusses our current understanding of the integrated intracellular and intercellular signaling networks that control plant growth.
Assuntos
Desenvolvimento Vegetal , Plantas/metabolismo , Meio Ambiente , Luz , Células Vegetais/metabolismo , Reguladores de Crescimento de Plantas/metabolismo , Raízes de Plantas/crescimento & desenvolvimento , Raízes de Plantas/metabolismo , Brotos de Planta/crescimento & desenvolvimento , Brotos de Planta/metabolismoRESUMO
The glycogen synthase kinase-3 (GSK3) family kinases are central cellular regulators highly conserved in all eukaryotes. In Arabidopsis, the GSK3-like kinase BIN2 phosphorylates a range of proteins to control broad developmental processes, and BIN2 is degraded through unknown mechanism upon receptor kinase-mediated brassinosteroid (BR) signaling. Here we identify KIB1 as an F-box E3 ubiquitin ligase that promotes the degradation of BIN2 while blocking its substrate access. Loss-of-function mutations of KIB1 and its homologs abolished BR-induced BIN2 degradation and caused severe BR-insensitive phenotypes. KIB1 directly interacted with BIN2 in a BR-dependent manner and promoted BIN2 ubiquitination in vitro. Expression of an F-box-truncated KIB1 caused BIN2 accumulation but dephosphorylation of its substrate BZR1 and activation of BR responses because KIB1 blocked BIN2 binding to BZR1. Our study demonstrates that KIB1 plays an essential role in BR signaling by inhibiting BIN2 through dual mechanisms of blocking substrate access and promoting degradation.
Assuntos
Proteínas de Arabidopsis/metabolismo , Arabidopsis/efeitos dos fármacos , Brassinosteroides/farmacologia , Proteínas F-Box/metabolismo , Quinase 3 da Glicogênio Sintase/metabolismo , Reguladores de Crescimento de Plantas/farmacologia , Plantas Geneticamente Modificadas/efeitos dos fármacos , Proteínas Quinases/metabolismo , Esteroides Heterocíclicos/farmacologia , Ubiquitina-Proteína Ligases/metabolismo , Arabidopsis/enzimologia , Arabidopsis/genética , Proteínas de Arabidopsis/genética , Sítios de Ligação , Domínio Catalítico , Proteínas de Ligação a DNA , Ativação Enzimática , Estabilidade Enzimática , Proteínas F-Box/genética , Genótipo , Quinase 3 da Glicogênio Sintase/genética , Mutação , Proteínas Nucleares/genética , Proteínas Nucleares/metabolismo , Fenótipo , Plantas Geneticamente Modificadas/enzimologia , Plantas Geneticamente Modificadas/genética , Complexo de Endopeptidases do Proteassoma/metabolismo , Ligação Proteica , Proteínas Quinases/genética , Proteólise , Transdução de Sinais/efeitos dos fármacos , Especificidade por Substrato , Ubiquitina-Proteína Ligases/genética , UbiquitinaçãoRESUMO
Chromatin configuration is critical for establishing tissue identity and changes substantially during tissue identity transitions. The crucial scientific and agricultural technology of in vitro tissue culture exploits callus formation from diverse tissue explants and tissue regeneration via de novo organogenesis. We investigated the dynamic changes in H3ac and H3K4me3 histone modifications during leaf-to-callus transition in Arabidopsis thaliana. We analyzed changes in the global distribution of H3ac and H3K4me3 during the leaf-to-callus transition, focusing on transcriptionally active regions in calli relative to leaf explants, defined by increased accumulation of both H3ac and H3K4me3. Peptide signaling was particularly activated during callus formation; the peptide hormones RGF3, RGF8, PIP1 and PIPL3 were upregulated, promoting callus proliferation and conferring competence for de novo shoot organogenesis. The corresponding peptide receptors were also implicated in peptide-regulated callus proliferation and regeneration capacity. The effect of peptide hormones in plant regeneration is likely at least partly conserved in crop plants. Our results indicate that chromatin-dependent regulation of peptide hormone production not only stimulates callus proliferation but also establishes pluripotency, improving the overall efficiency of two-step regeneration in plant systems.
Assuntos
Proteínas de Arabidopsis , Arabidopsis , Hormônios Peptídicos , Arabidopsis/metabolismo , Proteínas de Arabidopsis/metabolismo , Código das Histonas , Cromatina , Folhas de Planta/fisiologia , Regulação da Expressão Gênica de PlantasRESUMO
Leucine-rich repeat receptor kinases (LRR-RKs) play a pivotal role in diverse aspects of growth, development, and immunity in plants by sensing extracellular signals. Typically, LRR-RKs are activated through the ligand-induced interaction with a SOMATIC EMBRYOGENESIS RECEPTOR KINASE (SERK) coreceptor, triggering downstream signaling. ROOT MERISTEM GROWTH FACTOR1 (RGF1) INSENSITIVEs (RGIs) LRR-RLK receptors promote primary root meristem activity while inhibiting lateral root (LR) development in response to RGF peptide. In this study, we employed rapamycin-induced dimerization (RiD) and BAK1-INTERACTING RECEPTOR-LIKE KINASE3 (BIR3) chimera approaches to explore the gain-of-function of RGI1, RGI4, and RGI5. Rapamycin induced the association of cytosolic kinase domains (CKDs) of RGI1 and the BAK1 coreceptor, activating both mitogen-activated protein kinase 3 (MPK3) and MPK6. Rapamycin significantly inhibited LR formation in RiD-RGI1/RGI4/RGI5-BAK1 plants. Using transgenic Arabidopsis expressing RGI1CKD fused to the BIR3-LRR chimera under estradiol control, we observed a substantial reduction in LR density upon ß-estradiol treatment. Additionally, we identified a decrease in root gravitropism in BIR3 chimera plants. In contrast, RiD-RGI/BAK1 plants did not exhibit defects in root gravitropism, implying the importance of combinatorial interactions between RGIs and SERK coreceptors in the inhibition of root gravitropism. Constitutive activation of RGIs with BAK1 in RiD-RGI/BAK1 plants by rapamycin treatment resulted in the inhibition of primary root growth, resembling the inhibitory effects observed with high concentrations of phytohormones on primary root elongation. Our findings highlight that the interactions between CKDs of RGIs and BAK1, constitutively induced by rapamycin or BIR3 chimera, efficiently control LR development.
Assuntos
Proteínas de Arabidopsis , Arabidopsis , Proteínas Serina-Treonina Quinases/química , Proteínas Serina-Treonina Quinases/metabolismo , Proteínas Serina-Treonina Quinases/farmacologia , Proteínas de Arabidopsis/metabolismo , Dimerização , Plantas/metabolismo , Estradiol/metabolismo , Estradiol/farmacologiaRESUMO
Systemin, the first peptide hormone identified in plants, was initially isolated from tomato (Solanum lycopersicum) leaves. Systemin mediates local and systemic wound-induced defense responses in plants, conferring resistance to necrotrophic fungi and herbivorous insects. Systemin is recognized by the leucine-rich-repeat receptor-like kinase (LRR-RLK) receptor SYSTEMIN RECEPTOR1 (SYR1), but how the systemin recognition signal is transduced to intracellular signaling pathways to trigger defense responses is poorly understood. Here, we demonstrate that SERK family LRR-RLKs function as co-receptors for SYR1 to mediate systemin signal transduction in tomato. By using chemical genetic approaches coupled with engineered receptors, we revealed that the association of the cytoplasmic kinase domains of SYR1 with SERKs leads to their mutual trans-phosphorylation and the activation of SYR1, which in turn induces a wide range of defense responses. Systemin stimulates the association between SYR1 and all tomato SERKs (SlSERK1, SlSERK3A, and SlSERK3B). The resulting SYR1-SlSERK heteromeric complexes trigger the phosphorylation of TOMATO PROTEIN KINASE 1B (TPK1b), a receptor-like cytoplasmic kinase that positively regulates systemin responses. Additionally, upon association with SYR1, SlSERKs are cleaved by the Pseudomonas syringae effector HopB1, further supporting the finding that SlSERKs are activated by systemin-bound SYR1. Finally, genetic analysis using Slserk mutants showed that SlSERKs are essential for systemin-mediated defense responses. Collectively, these findings demonstrate that the systemin-mediated association of SYR1 and SlSERKs activates defense responses against herbivorous insects.
RESUMO
Plants adapt to high temperature stresses through thermomorphogenesis, a process that includes stem elongation and hyponastic leaf growth. Thermomorphogenesis is gated by the circadian clock through two evening-expressed clock components, TIMING OF CAB EXPRESSION1 (TOC1) and PSEUDO-RESPONSE REGULATORS5 (PRR5). These proteins directly interact with and inhibit PHYTOCHROME INTERACTING FACTOR4 (PIF4), a basic helix-loop-helix transcription factor that promotes thermoresponsive growth. PIF4-mediated thermoresponsive growth is positively regulated by ZEITLUPE (ZTL), a central clock component, but the molecular mechanisms underlying this are poorly understood. Here, we show that ZTL regulates thermoresponsive growth through TOC1 and PRR5. Genetic analyses reveal that ZTL regulates PIF4 activity as well as PIF4 expression. In Arabidopsis thaliana, ztl mutants exhibit highly accumulated TOC1 and PRR5 and unresponsive expression of PIF4 target genes under exposure to high temperatures. Mutations in TOC1 and PRR5 restore thermoactivation of PIF4 target genes and thermoresponsive growth in ztl mutants. We also show that the molecular chaperone heat-shock protein 90 promotes thermoresponsive growth through the ZTL-TOC1/PRR5 signaling module. Further, we show that ZTL protein stability is increased at high temperatures. Taken together, our results demonstrate that ZTL-mediated degradation of TOC1 and PRR5 enhances the sensitivity of hypocotyl growth to high temperatures.
Assuntos
Proteínas de Arabidopsis , Arabidopsis , Fatores de Transcrição/metabolismo , Proteínas de Arabidopsis/metabolismo , Ritmo Circadiano/fisiologia , Arabidopsis/metabolismo , Fatores de Transcrição Hélice-Alça-Hélice Básicos/genética , Fatores de Transcrição Hélice-Alça-Hélice Básicos/metabolismo , Regulação da Expressão Gênica de PlantasRESUMO
ROOT MERISTEM GROWTH FACTOR1 (RGF1) and its receptors RGF1 INSENSITIVEs (RGIs) regulate primary root meristem activity via a mitogen-activated protein kinase (MPK) signaling cascade in Arabidopsis. However, it is unknown how RGF1 regulates lateral root (LR) development. Here, we show that the RGF1-RGI1 peptide-receptor pair negatively regulates LR development via activation of PUCHI encoding AP2/EREBP. Exogenous RGF1 peptides inhibited LR development of the wild type. However, the rgi1 mutants were partially or fully insensitive to RGF1 during LR development, whereas four other rgi single mutants, namely rgi2, rgi3, rgi4, and rgi5, were sensitive to RGF1 in inhibiting LR formation. Consistent with this, the red fluorescent protein (RFP) signals driven by the RGF1 promoter were detected at stage I and the following stages, overlapping with RGI1 expression. PUCHI expression was significantly up-regulated by RGF1 but completely inhibited in rgi1. LR development of puchi1-1 was insensitive to RGF1. PUCHI expression driven by the RGI1 promoter reduced LR density in both the wild type and rgi1,2,3. Further, mpk6, but not mpk3, displayed significantly down-regulated PUCHI expression and insensitive LR development in response to RGF1. Collectively, these results suggest that the RGF1-RGI1 module negatively regulates LR development by activating PUCHI expression via MPK6.
Assuntos
Proteínas de Arabidopsis , Arabidopsis , Arabidopsis/metabolismo , Proteínas de Arabidopsis/metabolismo , Regulação da Expressão Gênica de Plantas , Meristema , Proteínas Quinases Ativadas por Mitógeno/genética , Proteínas Quinases Ativadas por Mitógeno/metabolismo , Peptídeos/metabolismo , Raízes de Plantas/metabolismo , Receptores de Peptídeos/metabolismo , Fatores de Transcrição/metabolismoRESUMO
Roots provide the plant with water and nutrients and anchor it in a substrate. Root development is controlled by plant hormones and various sets of transcription factors. Recently, various small peptides and their cognate receptors have been identified as controlling root development. Small peptides bind to membrane-localized receptor-like kinases, inducing their dimerization with co-receptor proteins for signaling activation and giving rise to cellular signaling outputs. Small peptides function as local and long-distance signaling molecules involved in cell-to-cell communication networks, coordinating root development. In this review, we survey recent advances in the peptide ligand-mediated signaling pathways involved in the control of root development in Arabidopsis. We describe the interconnection between peptide signaling and conventional phytohormone signaling. Additionally, we discuss the diversity of identified peptide-receptor interactions during plant root development.
Assuntos
Proteínas de Arabidopsis , Arabidopsis , Arabidopsis/genética , Arabidopsis/metabolismo , Proteínas de Arabidopsis/genética , Proteínas de Arabidopsis/metabolismo , Regulação da Expressão Gênica de Plantas , Meristema/metabolismo , Peptídeos/metabolismo , Raízes de Plantas/metabolismo , Transdução de SinaisRESUMO
Growth plasticity is a key mechanism by which plants adapt to the ever-changing environmental conditions. Since growth is a high-energy-demanding and irreversible process, it is expected to be regulated by the integration of endogenous energy status as well as environmental conditions. Here, we show that trehalose-6-phosphate (T6P) functions as a sugar signaling molecule that coordinates thermoresponsive hypocotyl growth with endogenous sugar availability. We found that the loss of T6P SYNTHASE 1 (TPS1) in Arabidopsis thaliana impaired high-temperature-mediated hypocotyl growth. Consistently, the activity of PIF4, a transcription factor that positively regulates hypocotyl growth, was compromised in the tps1 mutant. We further show that, in the tps1 mutant, a sugar signaling kinase KIN10 directly phosphorylates and destabilizes PIF4. T6P inhibits KIN10 activity in a GRIK-dependent manner, allowing PIF4 to promote hypocotyl growth at high temperatures. Together, our results demonstrate that T6P determines thermoresponsive growth through the KIN10-PIF4 signaling module. Such regulation of PIF4 by T6P integrates the temperature-signaling pathway with the endogenous sugar status, thus optimizing plant growth response to environmental stresses.
Assuntos
Arabidopsis/crescimento & desenvolvimento , Arabidopsis/metabolismo , Hipocótilo/crescimento & desenvolvimento , Hipocótilo/metabolismo , Transdução de Sinais , Fosfatos Açúcares/metabolismo , Temperatura , Trealose/análogos & derivados , Arabidopsis/efeitos dos fármacos , Arabidopsis/genética , Proteínas de Arabidopsis/metabolismo , Regulação da Expressão Gênica de Plantas/efeitos dos fármacos , Glucose/farmacologia , Modelos Biológicos , Morfogênese/efeitos dos fármacos , Complexo de Endopeptidases do Proteassoma/metabolismo , Ligação Proteica/efeitos dos fármacos , Estabilidade Proteica/efeitos dos fármacos , Proteólise/efeitos dos fármacos , Transdução de Sinais/efeitos dos fármacos , Sacarose/farmacologia , Trealose/metabolismoRESUMO
In plants, the steroidal hormone brassinosteroid (BR) regulates numerous developmental processes, including photomorphogenesis. Genetic, proteomic, and genomic studies in Arabidopsis have illustrated a fully connected BR signal transduction pathway from the cell surface receptor kinase BRI1 to the BZR1 family of transcription factors. Genome-wide analyses of protein-DNA interactions have identified thousands of BZR1 target genes that link BR signaling to various cellular, metabolic, and developmental processes, as well as other signaling pathways. In controlling photomorphogenesis, BR signaling is highly integrated with the light, gibberellin, and auxin pathways through both direct interactions between signaling proteins and transcriptional regulation of key components of these pathways. BR signaling also cross talks with other receptor kinase pathways to modulate stomata development and innate immunity. The molecular connections in the BR signaling network demonstrate a robust steroid signaling system that has evolved in plants to orchestrate signal transduction, genome expression, metabolism, defense, and development.
Assuntos
Proteínas de Arabidopsis/metabolismo , Arabidopsis/crescimento & desenvolvimento , Arabidopsis/metabolismo , Regulação da Expressão Gênica de Plantas , Proteínas Nucleares/metabolismo , Arabidopsis/genética , Arabidopsis/efeitos da radiação , Proteínas de Arabidopsis/genética , Proteínas de Ligação a DNA , Ativação Enzimática , Genes de Plantas , Giberelinas/genética , Giberelinas/metabolismo , Luz , Proteínas Nucleares/genética , Fotossíntese , Estômatos de Plantas/genética , Estômatos de Plantas/metabolismo , Mapeamento de Interação de Proteínas , Proteínas Quinases/genética , Proteínas Quinases/metabolismo , Receptor Cross-Talk , Transdução de Sinais , Transcrição GênicaRESUMO
A hierarchy of transcriptional regulators controlling lateral root formation in Arabidopsis thaliana has been identified, including the AUXIN RESPONSE FACTOR 7 (ARF7)/ARF19-LATERAL ORGAN BOUNDARIES DOMAIN 16 (LBD16)/LBD18 transcriptional network; however, their feedback regulation mechanisms are not known. Here we show that LBD18 controls ARF activity using the dual mode of a positive feedback loop. We showed that ARF7 and ARF19 directly bind AuxRE in the LBD18 promoter. A variety of molecular and biochemical experiments demonstrated that LBD18 binds a specific DNA motif in the ARF19 promoter to regulate its expression in vivo as well as in vitro. LBD18 interacts with ARFs including ARF7 and ARF19 via the Phox and Bem1 domain of ARF to enhance the transcriptional activity of ARF7 on AuxRE, and competes with auxin/indole-3-acetic acid (IAA) repressors for ARF binding, overriding the negative feedback loop exerted by Aux/IAA repressors. Taken together, these results show that LBD18 and ARFs form a double positive feedback loop, and that LBD18 uses the dual mode of a positive feedback loop by binding directly to the ARF19 promoter and through the protein-protein interactions with ARF7 and ARF19. This novel mechanism of feedback loops may constitute a robust feedback mechanism that ensures continued lateral root growth in response to auxin in Arabidopsis.
Assuntos
Proteínas de Arabidopsis/fisiologia , Arabidopsis/metabolismo , Regulação da Expressão Gênica de Plantas , Fatores de Transcrição/metabolismo , Fatores de Transcrição/fisiologia , Arabidopsis/genética , Arabidopsis/crescimento & desenvolvimento , Proteínas de Arabidopsis/metabolismo , Retroalimentação Fisiológica , Raízes de Plantas/crescimento & desenvolvimento , Raízes de Plantas/metabolismo , Regiões Promotoras Genéticas , Transcrição GênicaRESUMO
The trade-off between growth and immunity is crucial for survival in plants. However, the mechanism underlying growth-immunity balance has remained elusive. The PRE-IBH1-HBI1 tripartite helix-loop-helix/basic helix-loop-helix module is part of a central transcription network that mediates growth regulation by several hormonal and environmental signals. Here, genome-wide analyses of HBI1 target genes show that HBI1 regulates both overlapping and unique targets compared with other DNA binding components of the network in Arabidopsis thaliana, supporting a role in specifying network outputs and fine-tuning feedback regulation. Furthermore, HBI1 negatively regulates a subset of genes involved in immunity, and pathogen-associated molecular pattern (PAMP) signals repress HBI1 transcription. Constitutive overexpression and loss-of-function experiments show that HBI1 inhibits PAMP-induced growth arrest, defense gene expression, reactive oxygen species production, and resistance to pathogen. These results show that HBI1, as a component of the central growth regulation circuit, functions as a major node of crosstalk that mediates a trade-off between growth and immunity in plants.
Assuntos
Proteínas de Arabidopsis/metabolismo , Arabidopsis/crescimento & desenvolvimento , Arabidopsis/imunologia , Fatores de Transcrição Hélice-Alça-Hélice Básicos/metabolismo , Imunidade Vegetal , Receptores de Reconhecimento de Padrão/metabolismo , Arabidopsis/genética , Arabidopsis/microbiologia , Brassinosteroides/metabolismo , Flagelina/metabolismo , Regulação da Expressão Gênica de Plantas , Genes de Plantas , Modelos Biológicos , Imunidade Vegetal/genética , Ligação Proteica/genética , Receptores de Reconhecimento de Padrão/imunologia , Transdução de Sinais/genéticaRESUMO
Environmental and endogenous signals, including light, temperature, brassinosteroid (BR), and gibberellin (GA), regulate cell elongation largely by influencing the expression of the paclobutrazol-resistant (PRE) family helix-loop-helix (HLH) factors, which promote cell elongation by interacting antagonistically with another HLH factor, IBH1. However, the molecular mechanism by which PREs and IBH1 regulate gene expression has remained unknown. Here, we show that IBH1 interacts with and inhibits a DNA binding basic helix-loop-helix (bHLH) protein, HBI1, in Arabidopsis thaliana. Overexpression of HBI1 increased hypocotyl and petiole elongation, whereas dominant inactivation of HBI1 and its homologs caused a dwarf phenotype, indicating that HBI1 is a positive regulator of cell elongation. In vitro and in vivo experiments showed that HBI1 directly bound to the promoters and activated two EXPANSIN genes encoding cell wall-loosening enzymes; HBI1's DNA binding and transcriptional activities were inhibited by IBH1, but the inhibitory effects of IBH1 were abolished by PRE1. The results indicate that PREs activate the DNA binding bHLH factor HBI1 by sequestering its inhibitor IBH1. Altering each of the three factors affected plant sensitivities to BR, GA, temperature, and light. Our study demonstrates that PREs, IBH1, and HBI1 form a chain of antagonistic switches that regulates cell elongation downstream of multiple external and endogenous signals.
Assuntos
Proteínas de Arabidopsis/metabolismo , Arabidopsis/metabolismo , Fatores de Transcrição Hélice-Alça-Hélice Básicos/metabolismo , Arabidopsis/genética , Proteínas de Arabidopsis/genética , Fatores de Transcrição Hélice-Alça-Hélice Básicos/genética , Transdução de Sinais/genética , Transdução de Sinais/fisiologia , Fatores de Transcrição/genética , Fatores de Transcrição/metabolismoRESUMO
The circadian clock entrained by environmental light-dark cycles enables plants to fine-tune diurnal growth and developmental responses. Here, we show that physical interactions among evening clock components, including PSEUDO-RESPONSE REGULATOR 5 (PRR5), TIMING OF CAB EXPRESSION 1 (TOC1), and the Evening Complex (EC) component EARLY FLOWERING 3 (ELF3), define a diurnal repressive chromatin structure specifically at the PHYTOCHROME-INTERACTING FACTOR 4 (PIF4) locus in Arabidopsis. These three clock components act interdependently as well as independently to repress nighttime hypocotyl elongation, as hypocotyl elongation rate dramatically increased specifically at nighttime in the prr5-1 toc1-21 elf3-1 mutant, concomitantly with a substantial increase in PIF4 expression. Transcriptional repression of PIF4 by ELF3, PRR5, and TOC1 is mediated by the SWI2/SNF2-RELATED (SWR1) chromatin remodeling complex, which incorporates histone H2A.Z at the PIF4 locus, facilitating robust epigenetic suppression of PIF4 during the evening. Overall, these findings demonstrate that the PRR-EC-SWR1 complex represses hypocotyl elongation at night through a distinctive chromatin domain covering PIF4 chromatin.
RESUMO
Plants constantly face fluctuating ambient temperatures and must adapt to survive under stressful conditions. Temperature affects many aspects of plant growth and development through a complex network of transcriptional responses. Although temperature sensing is a crucial primary step in initiating transcriptional responses via Ca2+ and/or reactive oxygen species signaling, an understanding of how plants perceive temperature has remained elusive. However, recent studies have yielded breakthroughs in our understanding of temperature sensors and thermosensation mechanisms. We review recent findings on potential temperature sensors and emerging thermosensation mechanisms, including biomolecular condensate formation through phase separation in plants. We also compare the temperature perception mechanisms of plants with those of other organisms to provide insights into understanding temperature sensing by plants.
Assuntos
Desenvolvimento Vegetal , Plantas , Temperatura , Plantas/genética , Transdução de Sinais , PercepçãoRESUMO
In 1998, Bill Gray and colleagues showed that warm temperatures trigger arabidopsis hypocotyl elongation in an auxin-dependent manner. This laid the foundation for a vibrant research discipline. With several active members of the 'thermomorphogenesis' community, we here reflect on 25 years of elevated ambient temperature research and look to the future.
Assuntos
Proteínas de Arabidopsis , Arabidopsis , Proteínas de Arabidopsis/metabolismo , Regulação da Expressão Gênica de Plantas , Arabidopsis/genética , Arabidopsis/metabolismo , Temperatura , Hipocótilo/metabolismo , Ácidos IndolacéticosRESUMO
Thermomorphogenesis is the morphological response of plants to an elevation in the ambient temperature, which is mediated by the bHLH transcription factor PIF4. The evening-expressed clock component, PRR5, directly represses the expression of PIF4 mRNA. Additionally, PRR5 interacts with PIF4 protein and represses its transactivation activity, which in turn suppresses the thermoresponsive growth in the evening. Here, we found that the B-box zinc finger protein, BBX18, interacts with PRR5 through the B-Box2 domain. Deletion of the B-Box2 domain abolished the functions of BBX18, including the stimulation of PIF4 mRNA expression and hypocotyl growth. Overexpression of BBX18, and not of B-Box2-deleted BBX18, restored the expression of thermoresponsive genes in the evening. We further show that BBX18 prevents PRR5 from inhibiting PIF4-mediated high temperature responses. Taken together, our results suggest that BBX18 regulates thermoresponsive growth through the PRR5-PIF4 pathway.
RESUMO
Plant signaling peptides are involved in cell-cell communication networks and coordinate a wide range of plant growth and developmental processes. Signaling peptides generally bind to receptor-like kinases, inducing their dimerization with co-receptors for signaling activation to trigger cellular signaling and biological responses. Fertilization is an important life event in flowering plants, involving precise control of cell-cell communications between male and female tissues. Peptide-receptor-like kinase-mediated signaling plays an important role in male-female interactions for successful fertilization in flowering plants. Here, we describe the recent findings on the functions and signaling pathways of peptides and receptors involved in plant reproduction processes including pollen germination, pollen tube growth, pollen tube guidance to the embryo sac, and sperm cell reception in female tissues.
Assuntos
Tubo Polínico , Transdução de Sinais , Genes de Plantas , Peptídeos , Polinização , ReproduçãoRESUMO
Membrane-localized leucine-rich repeat receptor kinases (LRR-RKs) sense diverse extracellular signals, and coordinate and specify cellular functions in plants. However, functional understanding and identification of the cellular signaling of most LRR-RKs remain a major challenge owing to their genetic redundancy, the lack of ligand information, and subtle phenotypes of LRR-RK overexpression. Here, we report an engineered rapamycin-inducible dimerization (RiD) receptor system that triggers a receptor-specific LRR-RK signaling independent of their cognate ligands or endogenous receptors. Using the RiD-receptors, we demonstrated that the rapamycin-mediated association of chimeric cytosolic kinase domains from the BRI1/BAK1 receptor/co-receptor, but not the BRI1/BRI1 or BAK1/BAK1 homodimer, is sufficient to activate downstream brassinosteroid signaling and physiological responses. Furthermore, we showed that the engineered RiD-FLS2/BAK1 could activate flagellin-22-mediated immune signaling and responses. Using the RiD system, we also identified the potential function of an unknown orphan receptor in immune signaling and revealed the differential activities of SERK co-receptors of LRR-RKs. Our results indicate that the RiD method can serve as a synthetic biology tool for precise temporal manipulation of LRR-RK signaling and for understanding LRR-RK biology.