Arabidopsis Response Research Articles

Dephosphorylation of bZIP59 by PP2A ensures appropriate shade avoidance response in Arabidopsis.

Changes in light quality and quantity experienced by many shade-intolerant plants grown in close proximity lead to transcriptional reprogramming and shade avoidance syndrome (SAS). Despite the importance of phosphorylation-dependent signaling in cellular physiology, phosphorylation events during SAS are largely unknown. Here, we examined shade-regulated phosphorylation events in Arabidopsis using quantitative phosphoproteomics. We confirmed shade-induced dephosphorylation of bZIP59, a basic region/leucine zipper motif (bZIP) transcription factor. Shade treatment promotes the nuclear localization of bZIP59, which can be mimicked by mutation of the phosphorylation sites on bZIP59. Phenotypic analysis identified that bZIP59 negatively regulated shade-induced hypocotyl elongation. bZIP59 repressed the shade-induced activation of certain growth-related genes, while shade increased the DNA binding of bZIP59. Furthermore, the protein phosphatase 2A (PP2A) mediated dephosphorylation of bZIP59. Our study characterized a previously unidentified mechanism by which the phytochrome B (phyB)-PP2A-bZIP59 regulatory module integrates shade signals and transcriptomes, broadening our knowledge of phosphorylation strategies for rapid adaptation to shade.

Real-time monitoring of stromal NADPH levels in Arabidopsis using a metagenome-derived NADPH-binding fluorescent protein

The light irradiation to the plant chloroplasts drives NADPH and ATP synthesis in the stroma via the electron transport chains within the thylakoid membranes. Conventional methods for assessing photosynthetic light reactions are often invasive or require specific conditions. While detection markers do not significantly affect plant growth itself, developing a method for the real-time and non-invasive detection of NADPH is a highly impactful and important research area in plant physiology and biochemistry. This study introduces a genetically encoded NADPH-binding blue fluorescent protein (mBFP) targeted to the chloroplast stroma or thylakoid membrane in Arabidopsis thaliana and Nicotiana benthamiana. Using two-photon microscopy, we monitored real-time stromal NADPH levels in transgenic leaves of Arabidopsis in response to light exposure. A mutant mBFP construct targeted to the thylakoid membrane allowed us to detect the stromal NADPH levels in real time under different light conditions. This in planta biosensor provides a non-invasive tool for studying photosynthetic responses to light more quantitatively and holds potential for optimizing light conditions in controlled-environment agriculture, such as indoor vertical farms, to improve crop productivity.

HSFA1 heat shock factors integrate warm temperature and heat signals in plants

Warm temperatures and heat stress trigger distinct plant responses. Recently, Li et al. and Tan et al. identified HSFA1 heat shock transcription factors (HSFs) as central gatekeepers of high-temperature signaling, integrating warm temperature and heat shock responses (HSRs) in arabidopsis (Arabidopsis thaliana). HSFA1d stabilizes phytochrome-interacting factor 4 (PIF4) and activates HSFA2, establishing a crosstalk between thermomorphogenesis and thermotolerance.

Arabidopsis Actin-Binding Protein WLIM2A Links PAMP-Triggered Immunity and Cytoskeleton Organization.

Arabidopsis LIM proteins are named after the initials of three proteins Lin-11, Isl-1, and MEC-3, which belong to a class of transcription factors that play an important role in the developmental regulation of eukaryotes and are also involved in a variety of life processes, including gene transcription, the construction of the cytoskeleton, signal transduction, and metabolic regulation. Plant LIM proteins have been shown to regulate actin bundling in different cells, but their role in immunity remains elusive. Mitogen-activated protein kinases (MAPKs) are a family of conserved serine/threonine protein kinases that link upstream receptors to their downstream targets. Pathogens produce pathogen-associated molecular patterns (PAMPs) that trigger the activation of MAPK cascades in plants. Recently, we conducted a large-scale phosphoproteomic analysis of PAMP-induced Arabidopsis plants to identify putative MAPK targets. One of the identified phospho-proteins was WLIM2A, an Arabidopsis LIM protein. In this study, we investigated the role of WLIM2A in plant immunity. We employed a reverse-genetics approach and generated wlim2a knockout lines using CRISPR-Cas9 technology. We also generated complementation and phosphosite-mutated WLIM2A expression lines in the wlim2a background. The wlim2a lines were compromised in their response to Pseudomonas syringae Pst DC3000 but showed enhanced resistance to the necrotrophic fungus Botrytis cinereae. Transcriptome analyses of wlim2a mutants revealed the deregulation of immune hormone biosynthesis and signaling of salicylic acid (SA), jasmonic acid (JA), and ethylene (ET) pathways. The wlim2a mutants also exhibited altered stomatal phenotypes. Analysis of plants expressing WLIM2A variants of the phospho-dead or phospho-mimicking MAPK phosphorylation site showed opposing stomatal behavior and resistance phenotypes in response to Pst DC3000 infection, proving that phosphorylation of WLIM2A plays a crucial role in plant immunity. Overall, these data demonstrate that phosphorylation of WLIM2A by MAPKs regulates Arabidopsis responses to plant pathogens.

Mediator subunit 17 regulates light and darkness responses in Arabidopsis plants

Mediator 17 (MED17) is part of the head of the Mediator complex, which regulates transcription initiation in different eukaryotic organisms, including plants. We have previously characterized MED17 roles in Arabidopsis plants exposed to UV-B radiation, revealing its involvement in various aspects of the DNA damage response after exposure. med17 mutant plants showed altered HY5 expression, which encodes a transcription factor with a central role in photomorphogenesis. Our results demonstrate that med17 mutants show altered photomorphogenic responses and also to darkness, when compared to WT plants, and these differences could be due to altered expression of genes encoding key regulators of light and darkness signaling pathways, such as HY5, COP1 and PIF3. Moreover, med17 mutants exhibit transcriptome changes similar to those previously reported in plants exposed to red and blue light, as well as those previously described for photoreceptor mutants. Interestingly, med17 and hy5 mutants show a similar set of differentially expressed genes compared to WT plants, which suggests that both proteins may participate in a common light and dark-induced signaling pathways. Together, our data provides evidence that MED17 is an important regulator of the light and darkness responses in Arabidopsis.

Transcriptome analysis reveals role of transcription factor WRKY70 in early N-hydroxy-pipecolic acid signaling.

N-hydroxy-pipecolic acid (NHP) is a mobile metabolite essential for inducing and amplifying systemic acquired resistance (SAR) following pathogen attack. Early phases of NHP signaling leading to immunity have remained elusive. Here, we report the early transcriptional changes mediated by NHP and the role salicylic acid (SA) plays during this response in Arabidopsis (Arabidopsis thaliana). We show that distinct waves of expression within minutes to hours of NHP treatment include increased expression of WRKY transcription factor genes as the primary transcriptional response, followed by the induction of WRKY-regulated defense genes as the secondary response. Most genes induced by NHP within minutes were SA-dependent, whereas those induced within hours were SA-independent. These data suggest that NHP induces the primary transcriptional response under basal levels of SA and that new SA biosynthesis via ISOCHORISMATE SYNTHASE 1/SA-INDUCTION DEFICIT 2 (ICS1/SID2) is dispensable for inducing the secondary transcriptional response. We demonstrate that WRKY70 is required for the induced expression of a set of genes defining some of the secondary transcriptional response, SAR protection, and NHP-dependent enhancement of ROS production in response to flagellin treatment. Our study highlights the key genes and pathways defining early NHP responses and the role of WRKY70 in regulating NHP-dependent transcription.

Regulated cleavage and translocation of FERONIA control immunity in Arabidopsis roots.

Plant roots exhibit localized immunity (LI) mainly in the transition zone (TZ) and elongation zone (EZ). Plasma membrane-localized receptor-like kinases (RLKs) can mediate the plant's response to rhizosphere bacteria. However, how RLKs are involved in triggering LI in roots remains unclear. Here we identified dual actions for the RLK FERONIA (FER) in the LI response of Arabidopsis (Arabidopsis thaliana). The FER cytoplasmic domain is cleaved and translocated to the nucleus (FERN) to activate LI in the TZ and EZ in response to colonization by beneficial and pathogenic bacteria. In the absence or cessation of bacterial infection, full-length FER is plasma membrane-localized to maintain growth. Upon colonization and invasion by a high titre of bacteria, mature RAPID ALKALINIZATION FACTOR23 peptide accumulates and activates the matrix metalloproteinase At2-MMP, which triggers FER cytoplasmic domain cleavage specifically in the TZ and EZ to activate LI. This work demonstrates that two molecular forms of a single RLK balance growth and immunity via LI activation in Arabidopsis roots.

Wheat TaTIFY3B and TaTIFY10A play roles in seed germination and abiotic stress responses in transgenic Arabidopsis and rice

BackgroundSeed germination is a key process in the plant life cycle that affects the vegetative and reproductive stages of plants. Although the JAZ gene family has been characterized in many plants, the relationship between the JAZ gene and seed germination is still unclear.ResultsWe identified two members of the JAZ family from wheat, TaTIFY3B and TaTIFY10A. TaTIFY3B and TaTIFY10A were localized in both the cell membrane and nucleus. Spatio-temporal expression analysis of TaTIFY3B and TaTIFY10A in wheat revealed that these genes are essential for the preharvest sprouting (PHS) stage of seed development, with expression levels significantly decreasing during the ripening period. Transgenic rice plants overexpressing wheat TaTIFY3B and TaTIFY10A improved seed germination rates. Transgenic Arabidopsis plants overexpressing wheat TaTIFY10A improved seed germination rates and promoted flowering. In addition, abscisic acid (ABA) and jasmonic acid (JA) were found to induce TaTIFY3B and TaTIFY10A expression. Under different ABA concentrations, the seed germination rates of transgenic rice and Arabidopsis overexpressing TaTIFY3B and TaTIFY10A are superior to wild-type (WT) and mutant plants, and the root lengths of Arabidopsis overexpressing TaTIFY3B and TaTIFY10A also change. Under different JA concentrations, there is no difference in the seed germination rate of rice overexpressing TaTIFY3B and TaTIFY10A compared to WT and mutant plants, but there is a significant difference in the seed germination rate and root length of overexpressing Arabidopsis compared to WT and mutant plants. Under different concentrations of salt and drought treatments, the seed germination rate and root length of overexpressing Arabidopsis of TaTIFY3B and TaTIFY10A are affected.ConclusionsThis study offers a novel perspective for understanding the molecular basis of pre-harvest sprouting and provides potential candidate genes for controlling wheat seed germination.

ARR1 and ARR12 modulate arsenite toxicity responses in Arabidopsis roots by transcriptionally controlling the actions of NIP1;1 and NIP6;1.

Cytokinin is central to coordinating plant adaptation to environmental stresses. Here, we first demonstrated the involvement of cytokinin in Arabidopsis responses to arsenite [As(III)] stress. As(III) treatment reduced cytokinin contents, while cytokinin treatment repressed further primary root growth in Arabidopsis plants under As(III) stress. Subsequently, we revealed that the cytokinin signaling members ARR1 and ARR12, the type-B ARABIDOPSIS RESPONSE REGULATORs, participate in cytokinin signaling-mediated As(III) responses in plants as negative regulators. A comprehensive transcriptome analysis of the arr1 and arr12 single and arr1,12 double mutants was then performed to decipher the cytokinin signaling-mediated mechanisms underlying plant As(III) stress adaptation. Results revealed important roles for ARR1 and ARR12 in ion transport, nutrient responses, and secondary metabolite accumulation. Furthermore, using hierarchical clustering and regulatory network analyses, we identified two NODULIN 26-LIKE INTRINSIC PROTEIN (NIP)-encoding genes, NIP1;1 and NIP6;1, potentially involved in ARR1/12-mediated As(III) uptake and transport in Arabidopsis. By analyzing various combinations of arr and nip mutants, including high-order triple and quadruple mutants, we demonstrated that ARR1 and ARR12 redundantly function as negative regulators of As(III) tolerance by acting upstream of NIP1;1 and NIP6;1 to modulate their function in arsenic accumulation. ChIP-qPCR, EMSA, and transient dual-LUC reporter assays revealed that ARR1 and ARR12 transcriptionally activate the expression of NIP1;1 and NIP6;1 by directly binding to their promoters and upregulating their expression, leading to increased arsenic accumulation under As(III) stress. These findings collectively provide insights into cytokinin signaling-mediated plant adaptation to excessive As(III), contributing to the development of crops with low arsenic accumulation.

The perception and evolution of flagellin, cold shock protein and elongation factor Tu from vector-borne bacterial plant pathogens.

Vector-borne bacterial pathogens cause devastating plant diseases that cost billions of dollars in crop losses worldwide. These pathogens have evolved to be host- and vector-dependent, resulting in a reduced genome size compared to their free-living relatives. All known vector-borne bacterial plant pathogens belong to four different genera: 'Candidatus Liberibacter', 'Candidatus Phytoplasma', Spiroplasma and Xylella. To protect themselves against pathogens, plants have evolved pattern recognition receptors that can detect conserved pathogen features as non-self and mount an immune response. To gain an understanding of how vector-borne pathogen features are perceived in plants, we investigated three proteinaceous features derived from cold shock protein (csp22), flagellin (flg22) and elongation factor Tu (elf18) from vector-borne bacterial pathogens as well as their closest free-living relatives. In general, vector-borne pathogens have fewer copies of genes encoding flagellin and cold shock protein compared to their closest free-living relatives. Furthermore, epitopes from vector-borne pathogens were less likely to be immunogenic compared to their free-living counterparts. Most Liberibacter csp22 and elf18 epitopes do not trigger plant immune responses in tomato or Arabidopsis. Interestingly, csp22 from the citrus pathogen 'Candidatus Liberibacter asiaticus' triggers immune responses in solanaceous plants, while csp22 from the solanaceous pathogen 'Candidatus Liberibacter solanacearum' does not. Our findings suggest that vector-borne plant pathogenic bacteria evolved to evade host recognition.

The bifunctional transcription factor NAC32 modulates nickel toxicity responses through repression of root-nickel compartmentalization and activation of auxin biosynthesis

Nickel (Ni) is an important micronutrient, but excess Ni is toxic to many plant species. Currently, relatively little is known about the genetic basis of the plant responses to Ni toxicity. Here, we demonstrate that NAC32 transcription factor functions as a core genetic hub to regulate the Ni toxicity responses in Arabidopsis. NAC32 negatively regulates root-Ni concentration through the IREG2 (IRON REGULATED2) encoding a transporter. NAC32 also induces local auxin biosynthesis in the root-apex transition zone by upregulating YUCCA 7 (YUC7)/8/9 expression, which results in a local enhancement of auxin signaling in root tips, especially under Ni toxicity, thereby impaired primary root growth. By analyses of various combinations of nac32 and ireg2 mutants, as well as nac32 and yuc7/8/9 triple mutants, including high-order quadruple mutant, we demonstrated that NAC32 negatively regulates Ni stress tolerance by acting upstream of IREG2 and YUC7/8/9 to modulate their function in Ni toxicity responses. ChIPqPCR, EMSA (electrophoretic mobility shift assay) and transient dual-LUC reporter assays showed that NAC32 transcriptionally represses IREG2 expression but activates YUC7/8/9 expression by directly binding to their promoters. Our work demonstrates that NAC32 coordinates Ni compartmentation and developmental plasticity in roots, providing a conceptual framework for understanding Ni toxicity responses in plants.

Control of DNA demethylation by superoxide anion in plant stem cells.

Superoxide anion is thought to be a natural by-product with strong oxidizing ability in all living organisms and was recently found to accumulate in plant meristems to maintain stem cells in the shoot and undifferentiated meristematic cells in the root. Here we show that the DNA demethylase repressor of silencing 1 (ROS1) is one of the direct targets of superoxide in stem cells. The Fe-S clusters in ROS1 are oxidized by superoxide to activate its DNA glycosylase/lyase activity. We demonstrate that superoxide extensively participates in the establishment of active DNA demethylation in the Arabidopsis genome and that ARABIDOPSIS RESPONSE REGULATOR 12 acts downstream of ROS1-mediated superoxide signaling to maintain stem cell fate. Our results provide a mechanistic framework for superoxide control of the stem cell niche and demonstrate how redox and DNA demethylation interact to define stem cell fate in plants.

HASTY-mediated miRNA dynamics modulate nitrogen starvation-induced leaf senescence in Arabidopsis

Nitrogen (N) deficiency responses are essential for plant survival and reproduction. Here, via an expression genome-wide association study (eGWAS), we reveal a mechanism that regulates microRNA (miRNA) dynamics necessary for N deficiency responses in Arabidopsis. Differential expression levels of three NAC transcription factor (TF) genes involved in leaf N deficiency responses among Arabidopsis accessions are most significantly associated with polymorphisms in HASTY (HST), which encodes an importin/exportin family protein responsible for the generation of mature miRNAs. HST acts as a negative regulator of N deficiency-induced leaf senescence, and the disruption and overexpression of HST differently modifies miRNA dynamics in response to N deficiency, altering levels of miRNAs targeting transcripts. Interestingly, N deficiency prevents the interaction of HST with HST-interacting proteins, DCL1 and RAN1, and some miRNAs. This suggests that HST-mediated regulation of miRNA dynamics collectively controls regulations mediated by multiple N deficiency response-associated NAC TFs, thereby being central to the N deficiency response network.

Antisense transcription from stress-responsive transcription factors fine-tunes the cold response in Arabidopsis.

Transcription of antisense long noncoding RNAs (lncRNAs) occurs pervasively across eukaryotic genomes. Only a few antisense lncRNAs have been characterized and shown to control biological processes, albeit with idiosyncratic regulatory mechanisms. Thus, we largely lack knowledge about the general role of antisense transcription in eukaryotic organisms. Here, we characterized genes with antisense transcription initiating close to the poly(A) signal of genes (PAS genes) in Arabidopsis (Arabidopsis thaliana). We compared plant native elongation transcript sequencing (plaNET-seq) with RNA sequencing during short-term cold exposure and detected massive differences between the response in active transcription and steady-state levels of PAS gene-derived mRNAs. The cold-induced expression of transcription factors B-BOX DOMAIN PROTEIN28 (BBX28) and C2H2-TYPE ZINC FINGER FAMILY PROTEIN5 (ZAT5) was detected by plaNET-seq, while their steady-state level was only slightly altered due to high mRNA turnover. Knockdown of BBX28 and ZAT5 or of their respective antisense transcripts severely compromised plant freezing tolerance. Decreased antisense transcript expression levels resulted in a reduced cold response of BBX28 and ZAT5, revealing a positive regulatory role of both antisense transcripts. This study expands the known repertoire of noncoding transcripts. It highlights that native transcription approaches can complement steady-state RNA techniques to identify biologically relevant players in stress responses.

Sequestration of DBR1 to stress granules promotes lariat intronic RNAs accumulation for heat-stress tolerance

Heat stress (HS) poses a significant challenge to plant survival, necessitating sophisticated molecular mechanisms to maintain cellular homeostasis. Here, we identify SICKLE (SIC) as a key modulator of HS responses in Arabidopsis (Arabidopsis thaliana). SIC is required for the sequestration of RNA DEBRANCHING ENZYME 1 (DBR1), a rate-limiting enzyme of lariat intronic RNA (lariRNA) decay, into stress granules (SGs). The sequestration of DBR1 by SIC enhances the accumulation of lariRNAs, branched circular RNAs derived from excised introns during pre-mRNA splicing, which in turn promote the transcription of their parental genes. Our findings further demonstrate that SIC-mediated DBR1 sequestration in SGs is crucial for plant HS tolerance, as deletion of the N-terminus of SIC (SIC1–244) impairs DBR1 sequestration and compromises plant response to HS. Overall, our study unveils a mechanism of transcriptional regulation in the HS response, where lariRNAs are enriched through DBR1 sequestration, ultimately promoting the transcription of heat stress tolerance genes.

HIGH PLOIDY2-mediated SUMOylation of transcription factor ARR1 controls two-component signaling in Arabidopsis.

Cytokinins regulate plant growth, development, and responses to environmental stresses such as cold via phosphorelay from cytokinin receptors to the ARABIDOPSIS RESPONSE REGULATORs (ARRs). However, the molecular mechanisms underlying the activation of type-B ARR transcriptional activity in Arabidopsis (Arabidopsis thaliana) remain unclear. Here, we show that the E3 SUMO ligase HIGH PLOIDY2 SUMOylates ARR1, a type-B ARR, at K236, triggering its activation. Cold- or cytokinin-induced phosphorylation of ARR1 at D89 is crucial for its interaction with HPY2. Lysine 236 is critical for ARR1's transactivation without compromising its DNA-binding ability, while D89 is crucial for ARR1's binding to target gene promoters. Cytokinin enhances ARR1's chromatin binding, but cold does not. ARR1 K236 plays a critical role in promoting histone H3 acetylation in response to both cytokinin and cold without affecting chromatin binding. The K236R mutation in ARR1 reduces target gene expression and alters cytokinin and cold response phenotypes. This study unveils a mechanism of ARR1 activation wherein phosphorylated ARR1 interacts with HPY2 and binds to chromatin in response to cytokinin. Cold triggers a phosphorelay targeting chromatin-bound ARR1. HPY2 then catalyzes ARR1 SUMOylation at K236, enhancing histone H3 acetylation and leading to transcriptional activation of ARR1 in response to both cold and cytokinin.

Evaluating the effects of azelaic acid in the metabolism of Arabidopsis thaliana seedlings through untargeted metabolomics and ionomics approaches.

The present study demonstrates that low concentrations of azelaic acid (AZA) significantly impact the metabolism of Arabidopsis thaliana seedlings, leading to imbalances in numerous minerals and metabolites due to AZA-induced stress. Untargeted metabolomic analyses were conducted on untreated and AZA-treated seedlings at two time points: 7 and 14 days after treatment initiation. The results revealed a general accumulation of sugars (e.g., glucose, mannose, xylose), amino acids (e.g., lysine, GABA, threonine, glutamine), and organic acids (e.g., glutaric acid, shikimic acid, succinic acid) in AZA treated-seedlings, suggesting that AZA triggers stress responses in Arabidopsis. Ionomic analysis revealed that AZA induces phosphorus deficiency, which plants compensate by increasing malate content in the roots. Additionally, AZA treatment induced putrescine accumulation within the root, a metabolic biomarker of potassium deficiency and plant stress. The metabolomic profile showed elevated levels of different specialized metabolites, such as nitrogen- and sulphur-containing compounds, and altered levels of various phytohormones, including jasmonates and brassinosteroids, implicated in plant protection under biotic and/or abiotic stresses. These findings support the hypothesis that AZA's mode of action is associated with an auxin imbalance, suggesting its function as an auxinic herbicide. The observed increases in starch and jasmonates, coupled with the disruptions in potassium homeostasis, are linked to the previously reported alterations in the auxin transport, root architecture and gravitropic root response. Statistical analyses were applied, including Kruskal-Wallis tests for ionomic data, as well as multifactor analysis, Principal Component Analysis, Orthogonal Partial Least Squares-Discriminant Analysis, and enrichment pathway analysis for metabolomic data, ensuring the robustness and validity of these findings.

The Type III Effector XopLXcc in Xanthomonas campestris pv. campestris Targets the Proton Pump Interactor 1 and Suppresses Innate Immunity in Arabidopsis.

Xanthomonas campestris pathovar campestris (Xcc) is a significant phytopathogen causing black rot disease in crucifers. Xcc injects a variety of type III effectors (T3Es) into the host cell to assist infection or propagation. A number of T3Es inhibit plant immunity, but the biochemical basis for a vast majority of them remains unknown. Previous research has revealed that the evolutionarily conserved XopL-family effector XopLXcc inhibits plant immunity, although the underlying mechanisms remain incompletely elucidated. In this study, we identified proton pump interactor (PPI1) as a specific virulence target of XopLXcc in Arabidopsis. Notably, the C-terminus of PPI1 and the Leucine-rich repeat (LRR) domains of XopLXcc are pivotal for facilitating this interaction. Our findings indicate that PPI1 plays a role in the immune response of Arabidopsis to Xcc. These results propose a model in which XopLXcc binds to PPI1, disrupting the early defense responses activated in Arabidopsis during Xcc infection and providing valuable insights into potential strategies for regulating plasma membrane (PM) H+-ATPase activity during infection. These novel insights enhance our understanding of the pathogenic mechanisms of T3Es and contribute to the development of effective strategies for controlling bacterial diseases.

Genome-Wide Identification and Functional Analysis of the Genes of the ATL Family in Maize during High-Temperature Stress in Maize.

Maize is a significant food and feed product, and abiotic stress significantly impacts its growth and development. Arabidopsis Toxicosa en Levadura (ATL), a member of the RING-H2 E3 subfamily, modulates various physiological processes and stress responses in Arabidopsis. However, the role of ATL in maize remains unexplored. In this study, we systematically identified the genes encoding ATL in the maize genome. The results showed that the maize ATL family consists of 77 members, all predicted to be located in the cell membrane and cytoplasm, with a highly conserved RING domain. Tissue-specific expression analysis revealed that the expression levels of ATL family genes were significantly different in different tissues. Examination of the abiotic stress data revealed that the expression levels of ATL genes fluctuated significantly under different stress conditions. To further understand the biological functions of maize ATL family genes under high-temperature stress, we studied the high-temperature phenotypes of the maize ZmATL family gene ZmATL10 and its homologous gene AtATL27 in Arabidopsis. The results showed that overexpression of the ZmATL10 and AtATL27 genes enhanced resistance to high-temperature stress.

BAPID suppresses the inhibition of BRM on Di19-PR module in response to drought.

Drought is one of the most important abiotic stresses, and seriously threatens plant development and productivity. Increasing evidence indicates that chromatin remodelers are pivotal for plant drought response. However, molecular mechanisms of chromatin remodelers-mediated plant drought responses remain obscure. In this study, we found a novel interactor of BRM called BRM-associated protein involved in drought response (BAPID), which interacted with SWI/SNF chromatin remodeler BRM and drought-induced transcription factor Di19. Our findings demonstrated that BAPID acted as a positive drought regulator since drought tolerance was increased in BAPID-overexpressing plants, but decreased in BAPID-deficient plants, and physically bound to PR1, PR2, and PR5 promoters to mediate expression of PR genes to defend against dehydration stress. Genetic approaches demonstrated that BRM acted epistatically to BAPID and Di19 in drought response in Arabidopsis. Furthermore, the BAPID protein-inhibited interaction between BRM and Di19, and suppressed the inhibition of BRM on the Di19-PR module by mediating the H3K27me3 deposition at PR loci, thus changing nucleosome accessibility of Di19 and activating transcription of PR genes in response to drought. Our results shed light on the molecular mechanism whereby the BAPID-BRM-Di19-PRs pathway mediates plant drought responses. We provide data improving our understanding of chromatin remodeler-mediated plant drought regulation network.