Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

DET1 and COP1 Modulate the Coordination of Growth and Immunity in Response to Key Seasonal Signals in Arabidopsis.

ABSTRACT: Plant growth and development and outcomes of plant-microbe interactions are defined by coordinated responses to seasonal signals. The mechanisms that control the coordinated regulation of growth and immunity are not well understood. Here, we show that a common signaling module integrates environmental signals, such as photoperiod and temperature, to regulate the growth-defense balance. Key light-signaling components De-Etiolated 1 (DET1) and Constitutive Photomorphogenic 1 (COP1) negatively regulate immunity and are essential for immune modulation by photoperiod and temperature. Our results show that this is regulated by the transcription factor Phytochrome Interacting Factor 4 (PIF4), suggesting that the DET1/COP1-PIF4 module acts as a central hub for the control of growth and immunity in response to seasonal signals. These findings provide a regulatory framework for environmental signal integration.

SUBMITTER: Gangappa SN

PROVIDER: S-EPMC6180345 | biostudies-literature | 2018 Oct

REPOSITORIES: biostudies-literature

ACCESS DATA

Json Xml

Publications

DET1 and COP1 Modulate the Coordination of Growth and Immunity in Response to Key Seasonal Signals in Arabidopsis.

Gangappa Sreeramaiah N SN Kumar S Vinod SV

Cell reports 20181001 1

Plant growth and development and outcomes of plant-microbe interactions are defined by coordinated responses to seasonal signals. The mechanisms that control the coordinated regulation of growth and immunity are not well understood. Here, we show that a common signaling module integrates environmental signals, such as photoperiod and temperature, to regulate the growth-defense balance. Key light-signaling components De-Etiolated 1 (DET1) and Constitutive Photomorphogenic 1 (COP1) negatively regu ...[more]

PMID: 30282035

Similar Datasets

Mutant p53 protects ETS2 from non-canonical COP1/DET1 dependent degradation.

Project description:Mutations in the tumor suppressor gene TP53 contribute to the development of approximately half of all human cancers. One mechanism by which mutant p53 (mtp53) acts is through interaction with other transcription factors, which can either enhance or repress the transcription of their target genes. Mtp53 preferentially interacts with the erythroblastosis virus E26 oncogene homologue 2 (ETS2), an ETS transcription factor, and increases its protein stability. To study the mechanism underlying ETS2 degradation, we knocked down ubiquitin ligases known to interact with ETS2. We observed that knockdown of the constitutive photomorphogenesis protein 1 (COP1) and its binding partner De-etiolated 1 (DET1) significantly increased ETS2 stability, and conversely, their ectopic expression led to increased ETS2 ubiquitination and degradation. Surprisingly, we observed that DET1 binds to ETS2 independently of COP1, and we demonstrated that mutation of multiple sites required for ETS2 degradation abrogated the interaction between DET1 and ETS2. Furthermore, we demonstrate that mtp53 prevents the COP1/DET1 complex from ubiquitinating ETS2 and thereby marking it for destruction. Mechanistically, we show that mtp53 destabilizes DET1 and also disrupts the DET1/ETS2 complex thereby preventing ETS2 degradation. Our study reveals a hitherto unknown function in which DET1 mediates the interaction with the substrates of its cognate ubiquitin ligase complex and provides an explanation for the ability of mtp53 to protect ETS2.

| S-EPMC4914304 | biostudies-literature

Genetic interactions of Arabidopsis thaliana damaged DNA binding protein 1B (DDB1B) with DDB1A, DET1, and COP1.

Project description:Damaged DNA Binding protein 1 (DDB1)-CULLIN4 E3 ubiquitin ligase complexes have been implicated in diverse biological processes in a range of organisms. Arabidopsis thaliana encodes two homologs of DDB1, DDB1A, and DDB1B. In this study we use a viable partial loss of function allele of DDB1B, ddb1b-2, to examine genetic interactions with DDB1A, DET1 and COP1. Although the ddb1b-2 ddb1a double mutant is lethal, ddb1a ddb1b-2/+ and ddb1b-2 ddb1a/+ heterozygotes exhibit few developmental phenotypes but do exhibit decreased tolerance of ultraviolet light. In addition, germination in ddb1a and ddb1a ddb1b-2/+ was found to be sensitive to salt and mannitol, and both DDB1 single mutants as well as the heterozygotes exhibited heat sensitivity. DE-ETIOLATED1 (DET1) and CONSTITUTIVE PHOTOMORPHOGENIC1 (COP1) are negative regulators of light development which interact with DDB1-CUL4 complexes. Although ddb1a strongly enhances det1 phenotypes in both dark- and light-grown seedlings, ddb1b-2 weakly enhanced the det1 short hypocotyl phenotype in the dark, as well as enhancing anthocyanin levels and suppressing the det1 low chlorophyll phenotype in light-grown seedlings. In adults, ddb1a suppresses det1 early flowering and enhances the det1 dwarf phenotype. A similar trend was observed in ddb1b-2 det1 double mutants, although the effects were smaller in magnitude. In cop1 mutants, ddb1b-2 enhanced the cop1-4 short hypocotyl phenotype in dark and light, enhanced anthocyanin levels in cop1-1 in the light, but had no effect in adults. Thus the requirement for DDB1B varies in the course of development, from COP1-specific effects in hypocotyls to DET1-specific in adults.

| S-EPMC3583456 | biostudies-other

COP1/DET1/ETS axis regulates ERK transcriptome and sensitivity to MAPK inhibitors.

Project description:Aberrant activation of MAPK signaling leads to the activation of oncogenic transcriptomes. How MAPK signaling is coupled with the transcriptional response in cancer is not fully understood. In 2 MAPK-activated tumor types, gastrointestinal stromal tumor and melanoma, we found that ETV1 and other Pea3-ETS transcription factors are critical nuclear effectors of MAPK signaling that are regulated through protein stability. Expression of stabilized Pea3-ETS factors can partially rescue the MAPK transcriptome and cell viability after MAPK inhibition. To identify the players involved in this process, we performed a pooled genome-wide RNAi screen using a fluorescence-based ETV1 protein stability sensor and identified COP1, DET1, DDB1, UBE3C, PSMD4, and COP9 signalosome members. COP1 or DET1 loss led to decoupling between MAPK signaling and the downstream transcriptional response, where MAPK inhibition failed to destabilize Pea3 factors and fully inhibit the MAPK transcriptome, thus resulting in decreased sensitivity to MAPK pathway inhibitors. We identified multiple COP1 and DET1 mutations in human tumors that were defective in the degradation of Pea3-ETS factors. Two melanoma patients had de novo DET1 mutations arising after vemurafenib treatment. These observations indicate that MAPK signaling-dependent regulation of Pea3-ETS protein stability is a key signaling node in oncogenesis and therapeutic resistance to MAPK pathway inhibition.

| S-EPMC5873878 | biostudies-literature

Ethylene signals modulate the survival of Arabidopsis leaf explants.

Project description:BackgroundLeaf explants are major materials in plant tissue cultures. Incubation of detached leaves on phytohormone-containing media, which is an important process for producing calli and regenerating plants, change their cell fate. Although hormone signaling pathways related to cell fate transition have been widely studied, other molecular and physiological events occurring in leaf explants during this process remain largely unexplored.ResultsHere, we identified that ethylene signals modulate expression of pathogen resistance genes and anthocyanin accumulation in leaf explants, affecting their survival during culture. Anthocyanins accumulated in leaf explants, but were not observed near the wound site. Ethylene signaling mutant analysis revealed that ethylene signals are active and block anthocyanin accumulation in the wound site. Moreover, expression of defense-related genes increased, particularly near the wound site, implying that ethylene induces defense responses possibly by blocking pathogenesis via wounding. We also found that anthocyanin accumulation in non-wounded regions is required for drought resistance in leaf explants.ConclusionsOur study revealed the key roles of ethylene in the regulation of defense gene expression and anthocyanin biosynthesis in leaf explants. Our results suggest a survival strategy of detached leaves, which can be applied to improve the longevity of explants during tissue culture.

| S-EPMC10214724 | biostudies-literature

COP1 dynamics integrate conflicting seasonal light and thermal cues in the control of <i>Arabidopsis</i> elongation.

Project description:As the summer approaches, plants experience enhanced light inputs and warm temperatures, two environmental cues with an opposite morphogenic impact. Key components of this response are PHYTOCHROME B (phyB), EARLY FLOWERING 3 (ELF3), and CONSTITUTIVE PHOTOMORPHOGENIC 1 (COP1). Here, we used single and double mutant/overexpression lines to fit a mathematical model incorporating known interactions of these regulators. The fitted model recapitulates thermal growth of all lines used and correctly predicts thermal behavior of others not used in the fit. While thermal COP1 function is accepted to be independent of diurnal timing, our model shows that it acts at temperature signaling only during daytime. Defective response of cop1-4 mutants is epistatic to phyB-9 and elf3-8, indicating that COP1 activity is essential to transduce phyB and ELF3 thermosensory function. Our thermal model provides a unique toolbox to identify best allelic combinations enhancing climate change resilience of crops adapted to different latitudes.

| S-EPMC9390991 | biostudies-literature

COP1 destabilizes DELLA proteins in Arabidopsis.

Project description:DELLA transcriptional regulators are central components in the control of plant growth responses to the environment. This control is considered to be mediated by changes in the metabolism of the hormones gibberellins (GAs), which promote the degradation of DELLAs. However, here we show that warm temperature or shade reduced the stability of a GA-insensitive DELLA allele in Arabidopsis thaliana Furthermore, the degradation of DELLA induced by the warmth preceded changes in GA levels and depended on the E3 ubiquitin ligase CONSTITUTIVELY PHOTOMORPHOGENIC1 (COP1). COP1 enhanced the degradation of normal and GA-insensitive DELLA alleles when coexpressed in Nicotiana benthamiana. DELLA proteins physically interacted with COP1 in yeast, mammalian, and plant cells. This interaction was enhanced by the COP1 complex partner SUPRESSOR OF phyA-105 1 (SPA1). The level of ubiquitination of DELLA was enhanced by COP1 and COP1 ubiquitinated DELLA proteins in vitro. We propose that DELLAs are destabilized not only by the canonical GA-dependent pathway but also by COP1 and that this control is relevant for growth responses to shade and warm temperature.

| S-EPMC7306988 | biostudies-literature

Tissue signals imprint Aiolos expression in ILC2s to modulate type 2 immunity.

Project description:Group 2 innate lymphoid cells (ILC2s) manifest tissue heterogeneity and are crucial modulators of regional immune responses. The molecular mechanisms regulating tissue ILC2 properties remain elusive. Here, we interrogate the signatures of ILC2s from five tissues at the transcriptome and epigenetic level. We have found that tissue microenvironment strongly shapes ILC2 identities. The intestine induces Aiolos+ILC2s, whereas lung and pancreas enhance Galectin-1+ILC2s. Though being a faithful gut ILC2 feature under the steady state, Aiolos is induced in non-intestinal ILC2s by pro-inflammatory cytokines. Specifically, IL-33 stimulates Aiolos expression in both human and mouse non-intestinal ILC2s. Functionally, Aiolos facilitates eosinophil recruitment by supporting IL-5 production and proliferation of ST2+ILC2s through inhibiting PD-1. At the epigenetic level, ILC2 tissue characters are imprinted by open chromatin regions (OCRs) at non-promoters. Intestinal-specific transcription factor aryl hydrocarbon receptor (Ahr) binds to Ikzf3 (encoding Aiolos) locus, increases the accessibility of an intestinal ILC2-specific OCR, and promotes the Ikzf3 transcription by enhancing H3K27ac. Consequently, Ahr prevents ILC2s entering an "exhausted-like" state through sustaining Aiolos expression. Our work elucidates mechanism of ILC2 tissue adaptation and highlights Aiolos as a potential target of type 2 inflammation.

| S-EPMC8528704 | biostudies-literature

Long-range mobile signals mediate seasonal control of shoot growth.

Project description:In perennial plants, seasonal shifts provide cues that control adaptive growth patterns of the shoot apex. However, where these seasonal cues are sensed and communicated to the shoot apex remains unknown. We demonstrate that systemic signals from leaves play key roles in seasonal control of shoot growth in model tree hybrid aspen. Grafting experiments reveal that the tree ortholog of Arabidopsis flowering time regulator FLOWERING LOCUS T (FT) and the plant hormone gibberellic acid (GA) systemically convey seasonal cues to the shoot apex. GA (unlike FT) also acts locally in shoot apex, downstream of FT in seasonal growth control. At the shoot apex, antagonistic factors-LAP1, a target of FT and the FT antagonist TERMINAL FLOWER 1 (TFL1)-act locally to promote and suppress seasonal growth, respectively. These data reveal seasonal changes perceived in leaves that are communicated to the shoot apex by systemic signals that, in concert with locally acting components, control adaptive growth patterns.

| S-EPMC6561165 | biostudies-literature

Cryptochrome 2 competes with COP1 substrates to repress COP1 ubiquitin ligase activity during Arabidopsis photomorphogenesis.

Project description:In plants, the cryptochrome photoreceptors suppress the activity of the COP1/SPA ubiquitin ligase to initiate photomorphogenesis in blue light. Both CRY1 and CRY2 interact with the COP1/SPA complex in a blue light-dependent manner. The mechanisms underlying the inhibition of COP1 activity through direct interactions with photoactivated CRYs are not fully understood. Here we tested the hypothesis that CRY2 inhibits COP1 by displacing the degradation substrates from COP1. To this end, we analyzed the role of a conserved valine-proline (VP) motif in the C-terminal domain of CRY2 (CCT2), which resembles the core COP1-WD40-binding sequences present in the substrates of COP1. We show that the VP motif in CRY2 is essential for the interaction of CRY2 with COP1 in yeast two-hybrid assays and in planta Mutations in the VP motif of CRY2 abolished the CRY2 activity in photomorphogenesis, indicating the importance of VP. The interaction between COP1 and its VP-containing substrate PAP2 was prevented in the presence of coexpressed CRY2, but not in the presence of CRY2 carrying a VP mutation. Thus, since both PAP2 and CRY2 engage VP motifs to bind to COP1, these results demonstrate that CRY2 outcompetes PAP2 for binding to COP1. We further found that the previously unknown interaction between SPA1-WD and CCT2 occurs via the VP motif in CRY2, suggesting structural similarities in the VP-binding pockets of COP1-WD40 and SPA1-WD40 domains. A VP motif present in CRY1 is also essential for binding to COP1. Thus, CRY1 and CRY2 might share this mechanism of COP1 inactivation.

| S-EPMC6936435 | biostudies-literature

Arabidopsis COP1 SUPPRESSOR 2 Represses COP1 E3 Ubiquitin Ligase Activity through Their Coiled-Coil Domains Association.

Project description:CONSTITUTIVE PHOTOMORPHOGENIC 1 (COP1) functions as an E3 ubiquitin ligase and mediates a variety of developmental processes in Arabidopsis by targeting a number of key regulators for ubiquitination and degradation. Here, we identify a novel COP1 interacting protein, COP1 SUPPRESSOR 2 (CSU2). Loss of function mutations in CSU2 suppress the constitutive photomorphogenic phenotype of cop1-6 in darkness. CSU2 directly interacts with COP1 via their coiled-coil domains and is recruited by COP1 into nuclear speckles in living plant cells. Furthermore, CSU2 inhibits COP1 E3 ubiquitin ligase activity in vitro, and represses COP1 mediated turnover of HY5 in cell-free extracts. We propose that in csu2 cop1-6 mutants, the lack of CSU2's repression of COP1 allows the low level of COP1 to exhibit higher activity that is sufficient to prevent accumulation of HY5 in the dark, thus restoring the etiolated phenotype. In addition, CSU2 is required for primary root development under normal light growth condition.

| S-EPMC4694719 | 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