Inverse regulation of SOS1 and HKT1 protein localization and stability by SOS3/CBL4 in Arabidopsis thaliana.

To control net sodium (Na+) uptake, Arabidopsis plants utilize the plasma membrane (PM) Na+/H+ antiporter SOS1 to achieve Na+ efflux at the root and Na+ loading into the xylem, and the channel-like HKT1;1 protein that mediates the reverse flux of Na+ unloading off the xylem. Together, these opposing transport systems govern the partition of Na+ within the plant yet they must be finely co-regulated to prevent a futile cycle of xylem loading and unloading. Here, we show that the Arabidopsis SOS3 protein acts as the molecular switch governing these Na+ fluxes by favoring the recruitment of SOS1 to the PM and its subsequent activation by the SOS2/SOS3 kinase complex under salt stress, while commanding HKT1;1 protein degradation upon acute sodic stress. SOS3 achieves this role by direct and SOS2-independent binding to previously unrecognized functional domains of SOS1 and HKT1;1. These results indicate that roots first retain moderate amounts of salts to facilitate osmoregulation, yet when sodicity exceeds a set point, SOS3-dependent HKT1;1 degradation switches the balance toward Na+ export out of the root. Thus, SOS3 functionally links and co-regulates the two major Na+ transport systems operating in vascular plants controlling plant tolerance to salinity.

The HIGH EXPRESSION OF OSMOTICALLY RESPONSIVE GENE15-HISTONE DEACETYLASE9 complex associates with HYPONASTIC LEAVES 1 to modulate microRNA expression in response to abscisic acid signaling.

The regulation of microRNA (miRNA) biogenesis is crucial for maintaining plant homeostasis under biotic and abiotic stress. The crosstalk between the RNA polymerase II (Pol-II) complex and the miRNA processing machinery has emerged as a central hub modulating transcription and cotranscriptional processing of primary miRNA transcripts (pri-miRNAs). However, it remains unclear how miRNA-specific transcriptional regulators recognize MIRNA loci. Here, we show that the Arabidopsis (Arabidopsis thaliana) HIGH EXPRESSION OF OSMOTICALLY RESPONSIVE GENE15 (HOS15)-HISTONE DEACETYLASE9 (HDA9) complex is a conditional suppressor of miRNA biogenesis, particularly in response to abscisic acid (ABA). When treated with ABA, hos15/hda9 mutants show enhanced transcription of pri-miRNAs that is accompanied by increased processing, leading to overaccumulation of a set of mature miRNAs. Moreover, upon recognition of the nascent pri-miRNAs, the ABA-induced recruitment of the HOS15-HDA9 complex to MIRNA loci is guided by HYPONASTIC LEAVES 1 (HYL1). The HYL1-dependent recruitment of the HOS15-HDA9 complex to MIRNA loci suppresses expression of MIRNAs and processing of pri-miRNA. Most importantly, our findings indicate that nascent pri-miRNAs serve as scaffolds for recruiting transcriptional regulators, specifically to MIRNA loci. This indicates that RNA molecules can act as regulators of their own expression by causing a negative feedback loop that turns off their transcription, providing a self-buffering system.

S-acylated and nucleus-localized SALT OVERLY SENSITIVE3/CALCINEURIN B-LIKE4 stabilizes GIGANTEA to regulate Arabidopsis flowering time under salt stress.

The precise timing of flowering in adverse environments is critical for plants to secure reproductive success. We report a mechanism in Arabidopsis (Arabidopsis thaliana) controlling the time of flowering by which the S-acylation-dependent nuclear import of the protein SALT OVERLY SENSITIVE3/CALCINEURIN B-LIKE4 (SOS3/CBL4), a Ca2+-signaling intermediary in the plant response to salinity, results in the selective stabilization of the flowering time regulator GIGANTEA inside the nucleus under salt stress, while degradation of GIGANTEA in the cytosol releases the protein kinase SOS2 to achieve salt tolerance. S-acylation of SOS3 was critical for its nuclear localization and the promotion of flowering, but partly dispensable for salt tolerance. SOS3 interacted with the photoperiodic flowering components GIGANTEA and FLAVIN-BINDING, KELCH REPEAT, F-BOX1 and participated in the transcriptional complex that regulates CONSTANS to sustain the transcription of CO and FLOWERING LOCUS T under salinity. Thus, the SOS3 protein acts as a Ca2+- and S-acylation-dependent versatile regulator that fine-tunes flowering time in a saline environment through the shared spatial separation and selective stabilization of GIGANTEA, thereby connecting two signaling networks to co-regulate the stress response and the time of flowering.

The Na+/H+ antiporter SALT OVERLY SENSITIVE 1 regulates salt compensation of circadian rhythms by stabilizing GIGANTEA in Arabidopsis.

The circadian clock is a timekeeping, homeostatic system that temporally coordinates all major cellular processes. The function of the circadian clock is compensated in the face of variable environmental conditions ranging from normal to stress-inducing conditions. Salinity is a critical environmental factor affecting plant growth, and plants have evolved the SALT OVERLY SENSITIVE (SOS) pathway to acquire halotolerance. However, the regulatory systems for clock compensation under salinity are unclear. Here, we show that the plasma membrane Na+/H+ antiporter SOS1 specifically functions as a salt-specific circadian clock regulator via GIGANTEA (GI) in Arabidopsis thaliana. SOS1 directly interacts with GI in a salt-dependent manner and stabilizes this protein to sustain a proper clock period under salinity conditions. SOS1 function in circadian clock regulation requires the salt-mediated secondary messengers cytosolic free calcium and reactive oxygen species, pointing to a distinct regulatory role for SOS1 in addition to its function as a transporter to maintain Na+ homeostasis. Our results demonstrate that SOS1 maintains homeostasis of the salt response under high or daily fluctuating salt levels. These findings highlight the genetic capacity of the circadian clock to maintain timekeeping activity over a broad range of salinity levels.

The E3 ubiquitin ligase COP1 regulates salt tolerance via GIGANTEA degradation in roots.

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.

ABA INSENSITIVE 2 promotes flowering by inhibiting OST1/ABI5-dependent FLOWERING LOCUS C transcription in Arabidopsis.

The plant hormone abscisic acid (ABA) is an important regulator of plant growth and development and plays a crucial role in both biotic and abiotic stress responses. ABA modulates flowering time, but the precise molecular mechanism remains poorly understood. Here we report that ABA INSENSITIVE 2 (ABI2) is the only phosphatase from the ABA-signaling core that positively regulates the transition to flowering in Arabidopsis. Loss-of-function abi2-2 mutant shows significantly delayed flowering both under long day and short day conditions. Expression of floral repressor genes such as FLOWERING LOCUS C (FLC) and CYCLING DOF FACTOR 1 (CDF1) was significantly up-regulated in abi2-2 plants while expression of the flowering promoting genes FLOWERING LOCUS T (FT) and SUPPRESSOR OF OVEREXPRESSION OF CONSTANS 1 (SOC1) was down-regulated. Through genetic interactions we further found that ost1-3 and abi5-1 mutations are epistatic to abi2-2, as both of them individually rescued the late flowering phenotype of abi2-2. Interestingly, phosphorylation and protein stability of ABA INSENSITIVE 5 (ABI5) were enhanced in abi2-2 plants suggesting that ABI2 dephosphorylates ABI5, thereby reducing protein stability and the capacity to induce FLC expression. Our findings uncovered the unexpected role of ABI2 in promoting flowering by inhibiting ABI5-mediated FLC expression in Arabidopsis.

OsGADD45a1: a multifaceted regulator of rice architecture, grain yield, and blast resistance.

KEY MESSAGE: The homolog gene of the Growth Arrest and DNA Damage-inducible 45 (GADD45) in rice functions in the regulation of plant architecture, grain yield, and blast resistance. The Growth Arrest and DNA Damage-inducible 45 (GADD45) family proteins, well-established stress sensors and tumor suppressors in mammals, serve as pivotal regulators of genotoxic stress responses and tumorigenesis. In contrast, the homolog and role of GADD45 in plants have remained unclear. Herein, using forward genetics, we identified an activation tagging mutant AC13 exhibited dwarf characteristics resulting from the loss-of-function of the rice GADD45α homolog, denoted as OsGADD45a1. osgadd45a1 mutants displayed reduced plant height, shortened panicle length, and decreased grain yield compared to the wild-type Kitaake. Conversely, no obvious differences in plant height, panicle length, or grain yield were observed between wild-type and OsGADD45a1 overexpression plants. OsGADD45a1 displayed relatively high expression in germinated seeds and panicles, with localization in both the nucleus and cytoplasm. RNA-sequencing analysis suggested a potential role for OsGADD45a1 in the regulation of photosynthesis, and binding partner identification indicates OsGADD45a1 interacts with OsRML1 to regulate rice growth. Intriguingly, our study unveiled a novel role for OsGADD45a1 in rice blast resistance, as osgadd45a1 mutant showed enhanced resistance to Magnaporthe oryzae, and the expression of OsGADD45a1 was diminished upon blast fungus treatment. The involvement of OsGADD45a1 in rice blast fungus resistance presents a groundbreaking finding. In summary, our results shed light on the multifaceted role of OsGADD45a1 in rice, encompassing biotic stress response and the modulation of several agricultural traits, including plant height, panicle length, and grain yield.

The physiological role of thiol-based redox sensors in plant defense signaling.

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 H2 O2 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.

Plasma membrane-localized H+-ATPase OsAHA3 functions in saline-alkaline stress tolerance in rice.

KEY MESSAGE: A novel function of plasma membrane-localized H+-ATPase, OsAHA3, was identified in rice, which is involved in saline-alkaline tolerance and specifically responds to high pH during saline-alkaline stress. Saline-alkaline stress causes serious damage to crop production on irrigated land. Plants suffer more severe damage under saline-alkaline stress than under salinity stress alone. Plasma membrane-localized proton (H+) pump (H+-ATPase) is an important enzyme that controls plant growth and development by catalyzing H+ efflux and enabling effective charge balance. Many studies about the role of plasma membrane H+-ATPases in saline-alkaline stress tolerance have been reported in Arabidopsis, especially on the AtAHA2 (Arabidopsis thaliana H+-ATPase 2) gene; however, whether and how plasma membrane H+-ATPases play a role in saline-alkaline stress tolerance in rice remain unknown. Here, using the activation-tagged rice mutant pool, we found that the plasma membrane-localized H+-ATPase OsAHA3 (Oryza sativa autoinhibited H+-ATPase 3) is involved in saline-alkaline stress tolerance. Activation-tagged line 29 (AC29) was identified as a loss-of-function mutant of OsAHA3 and showed more severe growth retardation under saline-alkaline stress with high pH than under salinity stress. Moreover, osaha3 loss-of-function mutants generated by CRISPR/Cas9 system exhibited saline-alkaline stress sensitive phenotypes; staining of leaves with nitrotetrazolium blue chloride (NBT) and diaminobenzidine (DAB) revealed more reactive oxygen species (ROS) accumulation in osaha3 mutants. OsAHA3-overexpressing plants showed increased saline-alkaline stress tolerance than wild-type plants. Tissue-specific expression analysis revealed high expression level of OsAHA3 in leaf, sheath, glume, and panicle. Overall, our results revealed a novel function of plasma membrane-localized H+-ATPase, OsAHA3, which is involved in saline-alkaline stress tolerance and specifically responds to high pH.

Autophagy receptor OsNBR1 modulates salt stress tolerance in rice.

KEY MESSAGE: Autophagy receptor OsNBR1 modulates salt stress tolerance by affecting ROS accumulation in rice. The NBR1 (next to BRCA1 gene 1), as important selective receptors, whose functions have been reported in animals and plants. Although the function of NBR1 responses to abiotic stress has mostly been investigated in Arabidopsis thaliana, the role of NBR1 under salt stress conditions remains unclear in rice (Oryza sativa). In this study, by screening the previously generated activation-tagged line, we identified a mutant, activation tagging 10 (AC10), which exhibited salt stress-sensitive phenotypes. TAIL-PCR (thermal asymmetric interlaced PCR) showed that the AC10 line carried a loss-of-function mutation in the OsNBR1 gene. OsNBR1 was found to be a positive regulator of salt stress tolerance and was localized in aggregates. A loss-of-function mutation in OsNBR1 increased salt stress sensitivity, whereas overexpression of OsNBR1 enhanced salt stress resistance. The osnbr1 mutants showed higher ROS (reactive oxygen species) production, whereas the OsNBR1 overexpression (OsNBR1OE) lines showed lower ROS production, than Kitaake plants under normal and salt stress conditions. Furthermore, RNA-seq analysis revealed that expression of OsRBOH9 (respiratory burst oxidase homologue) was increased in osnbr1 mutants, resulting in increased ROS accumulation in osnbr1 mutants. Together our results established that OsNBR1 responds to salt stress by influencing accumulation of ROS rather than by regulating transport of Na+ and K+ in rice.

HOS15 is a transcriptional corepressor of NPR1-mediated gene activation of plant immunity.

Transcriptional regulation is a complex and pivotal process in living cells. HOS15 is a transcriptional corepressor. Although transcriptional repressors generally have been associated with inactive genes, increasing evidence indicates that, through poorly understood mechanisms, transcriptional corepressors also associate with actively transcribed genes. Here, we show that HOS15 is the substrate receptor for an SCF/CUL1 E3 ubiquitin ligase complex (SCFHOS15) that negatively regulates plant immunity by destabilizing transcriptional activation complexes containing NPR1 and associated transcriptional activators. In unchallenged conditions, HOS15 continuously eliminates NPR1 to prevent inappropriate defense gene expression. Upon defense activation, HOS15 preferentially associates with phosphorylated NPR1 to stimulate rapid degradation of transcriptionally active NPR1 and thus limit the extent of defense gene expression. Our findings indicate that HOS15-mediated ubiquitination and elimination of NPR1 produce effects contrary to those of CUL3-containing ubiquitin ligase that coactivate defense gene expression. Thus, HOS15 plays a key role in the dynamic regulation of pre- and postactivation host defense.

Plasma membrane-localized Hsp40/DNAJ chaperone protein facilitates OsSUVH7-OsBAG4-OsMYB106 transcriptional complex formation for OsHKT1;5 activation.

The salinization of irrigated land affects agricultural productivity. HIGH-AFFINITY POTASSIUM (K+ ) TRANSPORTER 1;5 (OsHKT1;5)-dependent sodium (Na+ ) transport is a key salt tolerance mechanism during rice growth and development. Using a previously generated high-throughput activation tagging-based T-DNA insertion mutant pool, we isolated a mutant exhibiting salt stress-sensitive phenotype, caused by a reduction in OsHKT1;5 transcripts. The salt stress-sensitive phenotype of this mutant results from the loss of function of OsDNAJ15, which encodes plasma membrane-localized heat shock protein 40 (Hsp40). osdnaj15 loss-of-function mutants show decreased plant height, increased leaf angle, and reduced grain number caused by shorter panicle length and fewer branches. On the other h'and, OsDNAJ15-overexpression plants showed salt stress-tolerant phenotypes. Intriguingly, salt stress facilitates the nuclear relocation of OsDNAJ15 so that it can interact with OsBAG4, and OsDNAJ15 and OsBAG4 synergistically facilitate the DNA-binding activity of OsMYB106 to positively regulate the expression of OsHKT1;5. Overall, our results reveal a novel function of plasma membrane-localized Hsp40 protein in modulating, alongside chaperon regulator OsBAG4, transcriptional regulation under salinity stress tolerance.

Redox-mediated structural and functional switching of C-repeat binding factors enhances plant cold tolerance.

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.

HOS15 Interacts with the Histone Deacetylase HDA9 and the Evening Complex to Epigenetically Regulate the Floral Activator GIGANTEA.

In plants, seasonal inputs such as photoperiod and temperature modulate the plant's internal genetic program to regulate the timing of the developmental transition from vegetative to reproductive growth. This regulation of the floral transition involves chromatin remodeling, including covalent modification of histones. Here, we report that HIGH EXPRESSION OF OSMOTICALLY RESPONSIVE GENE 15 (HOS15), a WD40 repeat protein, associates with a histone deacetylase complex to repress transcription of the GIGANTEA (GI)-mediated photoperiodic flowering pathway in Arabidopsis (Arabidopsis thaliana). Loss of function of HOS15 confers early flowering under long-day conditions because elevated GI expression. LUX ARRHYTHMO (LUX), a DNA binding transcription factor and component of the Evening Complex (EC), is important for the binding of HOS15 to the GI promoter. In wild type, HOS15 associates with the EC components LUX, EARLY FLOWERING 3 (ELF3), and ELF4 and the histone deacetylase HDA9 at the GI promoter, resulting in histone deacetylation and reduced GI expression. In the hos15-2 mutant, the levels of histone acetylation are elevated at the GI promoter, resulting in increased GI expression. Our data suggest that the HOS15-EC-HDA9 histone-modifying complex regulates photoperiodic flowering via the transcriptional repression of GI.

HEXOKINASE1 forms a nuclear complex with the PRC2 subunits CURLY LEAF and SWINGER to regulate glucose signaling.

The glucose sensor HEXOKINASE1 (HXK1) integrates myriad external and internal signals to regulate gene expression and development in Arabidopsis thaliana. However, how HXK1 mediates glucose signaling in the nucleus remains unclear. Here, using immunoprecipitation-coupled mass spectrometry, we show that two catalytic subunits of Polycomb Repressive Complex 2, SWINGER (SWN) and CURLY LEAF (CLF), directly interact with catalytically active HXK1 and its inactive forms (HXK1G104D and HXK1S177A ) via their evolutionarily conserved SANT domains. HXK1, CLF, and SWN target common glucose-responsive genes to regulate glucose signaling, as revealed by RNA sequencing. The glucose-insensitive phenotypes of the Arabidopsis swn-1 and clf-50 mutants were similar to that of hxk1, and genetic analysis revealed that CLF, SWN, and HXK1 function in the same genetic pathway. Intriguingly, HXK1 is required for CLF- and SWN-mediated histone H3 lysine 27 (H3K27me3) deposition and glucose-mediated gene repression. Moreover, CLF and SWN affect the recruitment of HXK1 to its target chromatin. These findings support a model in which HXK1 and epigenetic modifiers form a nuclear complex to cooperatively mediate glucose signaling, thereby affecting the histone modification and expression of glucose-regulated genes in plants.

SET DOMAIN GROUP 721 protein functions in saline-alkaline stress tolerance in the model rice variety Kitaake.

To isolate the genetic locus responsible for saline-alkaline stress tolerance, we developed a high-throughput activation tagging-based T-DNA insertion mutagenesis method using the model rice (Oryza sativa L.) variety Kitaake. One of the activation-tagged insertion lines, activation tagging 7 (AC7), showed increased tolerance to saline-alkaline stress. This phenotype resulted from the overexpression of a gene that encodes a SET DOMAIN GROUP 721 protein with H3K4 methyltransferase activity. Transgenic plants overexpressing OsSDG721 showed saline-alkaline stress-tolerant phenotypes, along with increased leaf angle, advanced heading and ripening dates. By contrast, ossdg721 loss-of-function mutants showed increased sensitivity to saline-alkaline stress characterized by decreased survival rates and reduction in plant height, grain size, grain weight and leaf angle. RNA sequencing (RNA-seq) analysis of wild-type Kitaake and ossdg721 mutants indicated that OsSDG721 positively regulates the expression level of HIGH-AFFINITY POTASSIUM (K+ ) TRANSPORTER1;5 (OsHKT1;5), which encodes a Na+ -selective transporter that maintains K+ /Na+ homeostasis under salt stress. Furthermore, we showed that OsSDG721 binds to and deposits the H3K4me3 mark in the promoter and coding region of OsHKT1;5, thereby upregulating OsHKT1;5 expression under saline-alkaline stress. Overall, by generating Kitaake activation-tagging pools, we established that the H3K4 methyltransferase OsSDG721 enhances saline-alkaline stress tolerance in rice.

The GIGANTEA-ENHANCED EM LEVEL Complex Enhances Drought Tolerance via Regulation of Abscisic Acid Synthesis.

Drought is one of the most critical environmental stresses limiting plant growth and crop productivity. The synthesis and signaling of abscisic acid (ABA), a key phytohormone in the drought stress response, is under photoperiodic control. GIGANTEA (GI), a key regulator of photoperiod-dependent flowering and the circadian rhythm, is also involved in the signaling pathways for various abiotic stresses. In this study, we isolated ENHANCED EM LEVEL (EEL)/basic Leu zipper 12, a transcription factor involved in ABA signal responses, as a GI interactor in Arabidopsis (Arabidopsis thaliana). The diurnal expression of 9-CIS-EPOXYCAROTENOID DIOXYGENASE 3 (NCED3), a rate-limiting ABA biosynthetic enzyme, was reduced in the eel, gi-1, and eel gi-1 mutants under normal growth conditions. Chromatin immunoprecipitation and electrophoretic mobility shift assays revealed that EEL and GI bind directly to the ABA-responsive element motif in the NCED3 promoter. Furthermore, the eel, gi-1, and eel gi-1 mutants were hypersensitive to drought stress due to uncontrolled water loss. The transcript of NCED3, endogenous ABA levels, and stomatal closure were all reduced in the eel, gi-1, and eel gi-1 mutants under drought stress. Our results suggest that the EEL-GI complex positively regulates diurnal ABA synthesis by affecting the expression of NCED3, and contributes to the drought tolerance of Arabidopsis.

Tomato PEPR1 ORTHOLOG RECEPTOR-LIKE KINASE1 Regulates Responses to Systemin, Necrotrophic Fungi, and Insect Herbivory.

Endogenous peptides regulate plant immunity and growth. Systemin, a peptide specific to the Solanaceae, is known for its functions in plant responses to insect herbivory and pathogen infections. Here, we describe the identification of the tomato (Solanum lycopersicum) PEPR1/2 ORTHOLOG RECEPTOR-LIKE KINASE1 (PORK1) as the TOMATO PROTEIN KINASE1b (TPK1b) interacting protein and demonstrate its biological functions in systemin signaling and tomato immune responses. Tomato PORK1 RNA interference (RNAi) plants with significantly reduced PORK1 expression showed increased susceptibility to tobacco hornworm (Manduca sexta), reduced seedling growth sensitivity to the systemin peptide, and compromised systemin-mediated resistance to Botrytis cinerea. Systemin-induced expression of Proteinase Inhibitor II (PI-II), a classical marker for systemin signaling, was abrogated in PORK1 RNAi plants. Similarly, in response to systemin and wounding, the expression of jasmonate pathway genes was attenuated in PORK1 RNAi plants. TPK1b, a key regulator of tomato defense against B. cinerea and M. sexta, was phosphorylated by PORK1. Interestingly, wounding- and systemin-induced phosphorylation of TPK1b was attenuated when PORK1 expression was suppressed. Our data suggest that resistance to B. cinerea and M. sexta is dependent on PORK1-mediated responses to systemin and subsequent phosphorylation of TPK1b. Altogether, PORK1 regulates tomato systemin, wounding, and immune responses.

HKT sodium and potassium transporters in Arabidopsis thaliana and related halophyte species.

High salinity induces osmotic stress and often leads to sodium ion-specific toxicity, with inhibitory effects on physiological, biochemical and developmental pathways. To cope with increased Na+ in soil water, plants restrict influx, compartmentalize ions into vacuoles, export excess Na+ from the cell, and distribute ions between the aerial and root organs. In this review, we discuss our current understanding of how high-affinity K+ transporters (HKT) contribute to salinity tolerance, focusing on HKT1-like family members primarily involved in long-distance transport, and in the recent research in the model plant Arabidopsis and its halophytic counterparts of the Eutrema genus. Functional characterization of the salt overly sensitive (SOS) pathway and HKT1-type transporters in these species indicate that they utilize similar approaches to deal with salinity, regardless of their tolerance.

Epigenetic switch from repressive to permissive chromatin in response to cold stress.

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.