Histone demethylase SlJMJ4 promotes leaf senescence via removal of H3K27 methylation of senescence-related genes in tomato
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ABSTRACT:
ORGANISM(S): Solanum lycopersicum
PROVIDER: GSE177487 | GEO | 2022/04/06
REPOSITORIES: GEO
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Project description:Histone demethylase SlJMJ4 promotes leaf senescence via removal of H3K27 methylation of senescence-related genes in tomato
| PRJNA737114 | ENA
Project description:We performed a transcriptomic analysis on two tomato genotypes, M82 and Tondo, in response to a PEG-mediated osmotic treatment, mimicking water stress. The analysis was conducted separately on leaves and roots to characterize the specific response of these two organs. A total of 6,267 differentially expressed transcripts related to osmotic stress response was detected. The construction of gene co-expression networks defined the metabolic and signaling pathways of the common and specific responses of leaf and root. The common response was characterized by ABA-dependent and ABA-independent signaling pathways, and by the interconnection between ABA and JA signaling. The root specific response concerned genes involved in cell wall metabolism and remodeling, whereas the leaf specific response was principally related to leaf senescence and ethylene signaling. The transcription factors representing the hubs of these regulatory networks were identified. Some of them have not yet characterized and can represent novel candidates for tolerance. Finally, several genes showing a genotype-specific expression regulation in response to the treatment were detected. These genes may be involved in the different sensitivity to the osmotic treatment of the two tomato genotypes. In conclusion, this work shed new light on the regulatory networks occurring in tomato leaf and root under osmotic stress and set the base for an in-depth characterization of novel stress-related genes, that may represent potential candidates for improving tolerance to water stress in tomato.
2023-05-15 | GSE224629 | GEO
Project description:Leaf senescence is governed by a complex regulatory network involving dynamic reprogramming of gene expression. Recent evidence indicates that trimethylation of histone H3 at lysine 4 (H3K4me3) alters gene expression during leaf senescence. However, it is largely unknown how histone modification is regulated in an age-dependent manner. We found that JMJ16, an Arabidopsis JmjC-domain containing protein, is a specific H3K4 demethylase that negatively regulates leaf senescence. The histone demethylase activity and the JmjN, JmjC, and FYR domains of JMJ16, but not the zf-C5HC2 domain, are essential for JMJ16 function in the regulation of leaf senescence. Genome-wide analysis revealed a widespread coordinated up-regulation of H3K4me3 and gene expression associated with leaf senescence in the loss-of-function jmj16 mutant compared with the wild type. Genetic analysis indicated that JMJ16 negatively regulates leaf senescence at least partly through repressing the expression of WRKY53 and SAG201, two known positive regulators of leaf senescence. Further analyses demonstrated that JMJ16 associates with WRKY53 and SAG201, and represses precocious expression of WRKY53 and SAG201 in mature leaves by reducing H3K4me3 levels at these loci. Moreover, association of JMJ16 on WRKY53 and SAG201 loci increased at mature stage but decreased at later stage, suggesting that the age-dependent dynamic chromatin association of JMJ16 is required for precise transcriptional activation of SAGs during leaf senescence. Thus, JMJ16 is an important regulator of leaf senescence that demethylates H3K4 at senescence-associated genes in an age-dependent manner.
2019-04-17 | GSE115362 | GEO
Project description:Leaf senescence can be triggered by jasmonic acid (JA) and darkness. There are scattered reports about JA and dark-induced senescence, respectively. While the precise regulatory mechanisms that integrate these two factors to initiate and regulate leaf senescence have not been identified. Here, we report a transcriptional regulating module centered on novel WRKY transcription factor that is responsible for both JA and dark-induced leaf senescence in tomato. The expression levels of SlWRKY37 together with the master transcription factor in JA signaling SlMYC2 could be significantly induced by both MeJA and dark treatments. SlMYC2 directly binds to the promoter of SlWRKY37 to active its expression. Knock out of SlWRKY37 inhibited JA and dark-induced leaf senescence. Transcriptome analysis revealed 1312 differentially expressed genes between slwrky37-CR and SlWRKY37-OE, including genes involved in JA synthesis as well as several senescence-associated genes (SAGs). We characterized SlWRKY53 and SlSGR1 as direct transcriptional targets of SlWRKY37 to regulate leaf senescence. Moreover, SlWRKY37 interacts with SlVQ7 protein in vivo and the interaction enhances its binding ability to the promoters and transcriptional activation to downstream target genes. In addition, SlWRKY37 is phosphorylated at the post-translational level. Phosphorylation of SlWRKY37 is essential for its protein interaction and transcriptional activation, indicating phosphorylation modification has a great effect on the function of SlWRKY37 protein. Our study reveals the physiological and molecular functions of SlWRKY37 in leaf senescence and offered a target gene to retard leaf yellowing by reducing the sensitivity to internal and external senescence signal such as JA and darkness.
2022-06-01 | GSE186072 | GEO
Project description:Basal branching in grasses, or tillering, is an important trait determining both form and function of crops. While similarities exist between eudicot and grass branching programs, one notable difference is that the tiller buds of grasses are covered by the subtending leaf, whereas eudicot buds are typically unconstrained. The current study shows that contact with the leaf sheath represses sorghum bud growth by providing a mechanical signal that cues the bud to refrain from rapid growth. Leaf removal resulted in massive reprogramming of the bud transcriptome that included signatures of epigenetic modifications, and also implicated several hormones in the response. Bud abscisic acid (ABA) transiently increased, then decreased following leaf removal relative to controls, and ABA was necessary to repress bud growth in the presence of the leaf. Jasmonic acid (JA) levels and signaling increased in buds following leaf removal. Remarkably, application of JA to buds in situ promoted growth. The repression of bud growth by leaf contact shares characteristics of thigmomorphogenic responses in other systems, including the involvement of JA, though the JA effect is opposite. The repression of bud growth by leaf contact may represent a mechanism to time tillering to an appropriate developmental stage of the plant.
2019-03-05 | GSE127822 | GEO
Project description:Leaf senescence is a highly coordinated and complicated process with the integration of numerous internal and environmental signals. Salicylic acid (SA) and reactive oxygen species (ROS) are two well-defined inducers of leaf senescence, whose contents progressively and inter-dependently increase during leaf senescence via a yet unknown mechanism. Here, we have characterized a newly identified positive regulator of leaf senescence, WRKY75, and demonstrated that knock-down or knock-out of WRKY75 delays, while over-expression of WRKY75 accelerates age-dependent leaf senescence. The WRKY75 transcription is induced by age, SA, H2O2, as well as multiple plant hormones. Meanwhile, WRKY75 is able to promote SA production by inducing the transcription of SA INDUCTION-DEFICIENT 2 (SID2), and suppress H2O2 scavenging partly by repressing the transcription of CATALASE 2 (CAT2). Genetic analysis reveals that the SID2 mutation or an increase of catalase activity rescues the precocious leaf senescence phenotype evoked by WRKY75 over-expression. Based on these results, we propose a “tripartite amplification loop” model in which WRKY75, SA and ROS undergo a gradual but self-sustained rise driven by three interlinked positive feedback regulations. This tripartite amplification loop provides a molecular framework connecting the upstream signals, such as age, ethylene, JA and ABA, to the downstream regulatory network executed by those SA-responsive and H2O2-responsive transcription factors during leaf senescence.
2017-11-07 | GSE102302 | GEO
Project description:We examined the transcriptome induced by GmNAC81 overexpression and leaf senescence and showed that GmNAC81 further modulates leaf senescence by regulating an extensive repertoire of functionally characterized senescence-associated genes (SAGs). GmNAC81 overexpression also uncovered the regulation of typical drought-responsive genes. Key regulators and effectors of ABA signaling were suppressed by GmNAC81 overexpression.
2020-10-24 | GSE159910 | GEO
Project description:The phytohormone abscisic acid (ABA) induces senescence and facilitates nutrient reuse, which are essential for increasing stress tolerance. Senescence controls plant aging and is closely associated with crop yield and quality. It is a complicated process finely tuned by multiple layers of control. A significant proportion of ABA-responsive genes and cis-elements are targeted by H3K27me3 modification that is mediated by Polycomb group proteins (PcGs); however, the interplay between the major epigenetic machinery and the central stress hormone is poorly understood. Both pathways influence the transcription of thousands of genes, and the dynamic and quantitative epigenomic and transcriptomic changes cannot be characterized with high confidence. This issue is further complicated by the redundant roles of PcG components. This article revealed an intriguing mechanism of the interplay between ABA and PcG in regulating plant senescence, based on the integration of genetic evidence and quantitative comparison of epigenomic data derived from a purpose-developed computational model. We observed that >30% of ABA-induced genes are up-regulated in a double mutant of H3K27me3 methyltransferases CLF and SWN; and the double mutant, but not single-gene mutants, is hyper-sensitive to ABA treatment. Importantly, ABA-triggered H3K27me3 reduction preferentially occurred in regions around senescence-associated genes (SAGs), which are redundantly repressed by CLF and SWN in normal conditions. Furthermore, we revealed that the presence of H3K27me3 surrounding SAGs does not block ABA-induced SAG expression, but rather limits the extent of the induction, thereby preventing an over-sensitive response within a dynamic environment. These findings may serve as a paradigm for the crosstalk between the rapid-effect of phytohormone and the long-term effect of epigenetic machinery in regulating plant environmental responses through modulations of the senescence process.
2018-12-14 | GSE98301 | GEO
Project description:To identify marker genes that are specific for N starvation-induced leaf senescence and suitable to detect cultivar differences at early senescence stages prior to chlorophyll loss, the transcriptomes of leaves of two B. napus cultivars differing in stay-green characteristics and N efficiency were analysed four days after senescence induction by the senescence inducers N starvation, leaf shading and leaf detaching.
2015-01-15 | GSE60108 | GEO
Project description:Leaf senescence is a developmental process designed for nutrient recycling and relocation to maximize growth competence and reproductive capacity of plants. Thus, plants integrate developmental and environmental signals to precisely control senescence. However, it remains largely elusive as to how plants coordinate genetic, epigenetic, and metabolic pathways for the regulation of senescence. To genetically dissect the complex regulatory mechanism underlying leaf senescence, we identified an early leaf senescence mutant, rse1. RSE1 encodes a putative glycosyltranferase. Loss-of-function mutations in RSE1 resulted in precocious leaf yellowing and up-regulation of senescence maker genes, indicating enhanced leaf senescence. Transcriptome analysis revealed that salicylic acid (SA) and defense signaling cascades were activated in rse1 prior to the onset of leaf senescence. In agreement with the phenotypes, we found that SA accumulation was significantly increased in rse1. We also discovered that the rse1 phenotypes are dependent on SA-INDUCTION DEFICIENT 2 (SID2), indicating a role of SA in accelerated leaf senescence in rse1. Furthermore, RSE1 protein was localized to the cell walls, and rse1 displayed increased glucose contents in the cell walls, implying a possible link between the cell walls and RSE1 function. Together, we show that RSE1 negatively modulate leaf senescence through an SID2-dependent SA signaling pathway.
2019-10-18 | GSE132740 | GEO