Many studies have been conducted to understand plant stress responses to salinity because irrigation-dependent salt accumulation compromises crop productivity and also to understand the mechanism ...through which some plants thrive under saline conditions. As mechanistic understanding has increased during the last decades, discovery-oriented approaches have begun to identify genetic determinants of salt tolerance. In addition to osmolytes, osmoprotectants, radical detoxification, ion transport systems, and changes in hormone levels and hormone-guided communications, the Salt Overly Sensitive (SOS) pathway has emerged to be a major defense mechanism. However, the mechanism by which the components of the SOS pathway are integrated to ultimately orchestrate plant-wide tolerance to salinity stress remains unclear. A higher-level control mechanism has recently emerged as a result of recognizing the involvement of GIGANTEA (GI), a protein involved in maintaining the plant circadian clock and control switch in flowering. The loss of GI function confers high tolerance to salt stress via its interaction with the components of the SOS pathway. The mechanism underlying this observation indicates the association between GI and the SOS pathway and thus, given the key influence of the circadian clock and the pathway on photoperiodic flowering, the association between GI and SOS can regulate growth and stress tolerance. In this review, we will analyze the components of the SOS pathways, with emphasis on the integration of components recognized as hallmarks of a halophytic lifestyle.
Summary
Plants have developed multilayered defense strategies to adapt and acclimate to the kaleidoscopic environmental changes that rapidly produce reactive oxygen species (ROS) and induce redox ...changes. Thiol‐based redox sensors containing the redox‐sensitive cysteine residues act as the central machinery in plant defense signaling. Here, we review recent research on thiol‐based redox sensors in plants, which perceive the changes in intracellular H2O2 levels and activate specific downstream defense signaling. The review mainly focuses on the molecular mechanism of how the thiol sensors recognize internal/external stresses and respond to them by demonstrating several instances, such as cold‐, drought‐, salinity‐, and pathogen‐resistant signaling pathways. Also, we introduce another novel complex system of thiol‐based redox sensors operating through the liquid–liquid phase separation.
Aedes aegypti is a major vector of dengue fever in tropical regions. Spatial repellents (SRs) have shown promise in delaying pesticide resistance. Methods for discriminating concentrations (DCs) are ...well established using various bioassay tools, while data for high-throughput screening system (HITSS) toxicity bioassay (TOX) are absent. In this study, we compared and optimized lethal (LCs) and sub-lethal concentrations (SLCs) of transfluthrin (TFT) and metofluthrin (MFT) on pyrethroid-susceptible (USDA) and pyrethroid-resistant (Pu-Teuy) Ae. aegypti (L.) strains, using the HITSS-TOX. Mean mortality (MT) was 100% at LC99 and DC, compared to LC50 (45.0 ± 3.7%) and LC75 (65.8 ± 7.0%) for the USDA strain. However, the resistant strain (Pu-Teuy) showed reduced susceptibility against TFT and a significantly lower MT at LC50 (12.5 ± 4.4%; t = 5.665, df = 10, p < 0.001), LC75 (9.2 ± 3.5%; t = 4.844, df = 10, p = 0.001), LC99 (55.0 ± 9.9%; t = 4.538, df = 5, p = 0.006), and DC (75.0 ± 5.2%; U = 3.0, p = 0.007). The DC of TFT (0.15222%) was 4.7-fold higher than for MFT (0.03242%) in USDA strain. The baseline DCs established are useful to better understand susceptibility and the efficacy of various repellents against field populations of Ae. aegypti.
Switching from repressed to active status in chromatin regulation is part of the critical responses that plants deploy to survive in an ever-changing environment. We previously reported that HOS15, a ...WD40-repeat protein, is involved in histone deacetylation and cold tolerance in Arabidopsis. However, it remained unknown how HOS15 regulates cold responsive genes to affect cold tolerance. Here, we show that HOS15 interacts with histone deacetylase 2C (HD2C) and both proteins together associate with the promoters of cold-responsive COR genes, COR15A and COR47. Cold induced HD2C degradation is mediated by the CULLIN4 (CUL4)-based E3 ubiquitin ligase complex in which HOS15 acts as a substrate receptor. Interference with the association of HD2C and the COR gene promoters by HOS15 correlates with increased acetylation levels of histone H3. HOS15 also interacts with CBF transcription factors to modulate cold-induced binding to the COR gene promoters. Our results here demonstrate that cold induces HOS15-mediated chromatin modifications by degrading HD2C. This switches the chromatin structure status and facilitates recruitment of CBFs to the COR gene promoters. This is an apparent requirement to acquire cold tolerance.
Investigation of the endoplasmic reticulum-associated degradation (ERAD) system in plants led to the identification of ERAD-mediating RING finger protein (EMR) as a plant-specific ERAD E3 ligase from ...Arabidopsis. EMR was significantly up-regulated under endoplasmic reticulum (ER) stress conditions.
The EMR protein purified from bacteria displayed high E3 ligase activity, and tobacco leaf-produced EMR mediated mildew resistance locus O-12 (MLO12) degradation in a proteasome-dependent manner.
Subcellular localization and coimmunoprecipitation analyses showed that EMR forms a complex with ubiquitin-conjugating enzyme 32 (UBC32) as a cytosolic interaction partner. Mutation of EMR and RNA interference (RNAi) increased the tolerance of plants to ER stress. EMR RNAi in the bri1-5 background led to partial recovery of the brassinosteroid (BR)-insensitive phenotypes as compared with the original mutant plants and increased ER stress tolerance.
The presented results suggest that EMR is involved in the plant ERAD system that affects BR signaling under ER stress conditions as a novel Arabidopsis ring finger E3 ligase mainly present in cytosol while the previously identified ERAD E3 components are typically membrane-bound proteins.
Summary
C‐repeat binding factors (CBFs) are key cold‐responsive transcription factors that play pleiotropic roles in the cold acclimation, growth, and development of plants. Cold‐sensitive cbf ...knockout mutants and cold‐tolerant CBF overexpression lines exhibit abnormal phenotypes at warm temperatures, suggesting that CBF activity is precisely regulated, and a critical threshold level must be maintained for proper plant growth under normal conditions. Cold‐inducible CBFs also exist in warm‐climate plants but as inactive disulfide‐bonded oligomers. However, upon translocation to the nucleus under a cold snap, the h2‐isotype of cytosolic thioredoxin (Trx‐h2), reduces the oxidized (inactive) CBF oligomers and the newly synthesized CBF monomers, thus producing reduced (active) CBF monomers. Thus, the redox‐dependent structural switching and functional activation of CBFs protect plants under cold stress.
Excess soil salinity significantly impairs plant growth and development. Our previous reports demonstrated that the core circadian clock oscillator GIGANTEA (GI) negatively regulates salt stress ...tolerance by sequestering the SALT OVERLY SENSITIVE (SOS) 2 kinase, an essential component of the SOS pathway. Salt stress induces calcium‐dependent cytoplasmic GI degradation, resulting in activation of the SOS pathway; however, the precise molecular mechanism governing GI degradation during salt stress remains enigmatic. Here, we demonstrate that salt‐induced calcium signals promote the cytoplasmic partitioning of CONSTITUTIVE PHOTOMORPHOGENIC 1 (COP1), leading to the 26S proteasome‐dependent degradation of GI exclusively in the roots. Salt stress‐induced calcium signals accelerate the cytoplasmic localization of COP1 in the root cells, which targets GI for 26S proteasomal degradation. Align with this, the interaction between COP1 and GI is only observed in the roots, not the shoots, under salt‐stress conditions. Notably, the gi‐201 cop1‐4 double mutant shows an enhanced tolerance to salt stress similar to gi‐201, indicating that GI is epistatic to COP1 under salt‐stress conditions. Taken together, our study provides critical insights into the molecular mechanisms governing the COP1‐mediated proteasomal degradation of GI for salt stress tolerance, raising new possibilities for developing salt‐tolerant crops.
Summary statement
Salt‐induced Ca2+ signal triggers E3 ubiquitin ligase CONSTITUTIVE PHOTOMORPHOGENIC 1 (COP1) dependent proteasomal degradation of cytosolic GIGANTEA (GI) in the roots under salt‐stress conditions. Consequently, COP1‐regulated GI degradation positively regulates salt stress tolerance in Arabidopsis thaliana.
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