Glycosyltransferase-like RSE1 negatively regulates leaf senescence by modulating salicylic acid signaling in Arabidopsis
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ABSTRACT:
PROVIDER: PRJNA548877 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR9302510_1.fastq.gz | Fastqsanger.gz | |||
| SRR9302510_2.fastq.gz | Fastqsanger.gz | |||
| SRR9302511_1.fastq.gz | Fastqsanger.gz | |||
| SRR9302511_2.fastq.gz | Fastqsanger.gz | |||
| SRR9302512_1.fastq.gz | Fastqsanger.gz |
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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
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. To genetically dissect the complex regulatory mechanism underlying leaf senescence, we identified an early leaf senescence mutant, rse1. RSE1 encodes a putative glycosyltransferase. Loss-of-function mutations in RSE1 resulted in precocious leaf yellowing and up-regulation of senescence marker genes, indicating enhanced leaf senescence. Transcriptome analysis revealed that salicylic acid (SA) and defense signaling cascades were up-regulated in rse1 prior to the onset of leaf senescence. We found that SA accumulation was significantly increased in rse1. The rse1 phenotypes are dependent on SA-INDUCTION DEFICIENT 2 (SID2), supporting a role of SA in accelerated leaf senescence in rse1. Furthermore, RSE1 protein was localized to the cell wall, implying a possible link between the cell wall and RSE1 function. Together, we show that RSE1 negatively modulates leaf senescence through an SID2-dependent SA signaling pathway.
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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.
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Project description:Epigenetic alterations are among the prominent drivers of cellular senescence and/or aging. In this study, we show that histone lactylation plays a pivotal role in counteracting senescence and mitigating dysfunctions of skeletal muscle in aged mice. Mechanistically, histone lactylation and lactyl-CoA levels markedly decrease during cellular senescence but are restored under hypoxic conditions primarily due to elevated glycolytic activity. The enrichment of histone lactylation at promoters is essential for sustaining the expression of genes involved in the cell cycle and DNA repair pathways, thereby inhibiting cellular senescence. Furthermore, the modulation of enzymes crucial for histone lactylation, including p300 and HDAC1, leads to reduced histone lactylation and accelerated cellular senescence. Consistently, the suppression of glycolysis and the depletion of histone lactylation are also observed during skeletal muscle aging. Modulating the enzymes also leads to the loss of histone lactylation in skeletal muscle, downregulating DNA repair and proteostasis pathways and accelerating muscle aging. Running exercise increases the levels of glycolysis and histone lactylation, thereby helping to preserve the proper function of skeletal muscle. Our study highlights the significant roles of histone lactylation in modulating cellular senescence and muscle aging, suggesting that this modification may serve as an innovative biomarker for senescence.
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Project description:Epigenetic alterations are among the prominent drivers of cellular senescence and/or aging. In this study, we show that histone lactylation plays a pivotal role in counteracting senescence and mitigating dysfunctions of skeletal muscle in aged mice. Mechanistically, histone lactylation and lactyl-CoA levels markedly decrease during cellular senescence but are restored under hypoxic conditions primarily due to elevated glycolytic activity. The enrichment of histone lactylation at promoters is essential for sustaining the expression of genes involved in the cell cycle and DNA repair pathways, thereby inhibiting cellular senescence. Furthermore, the modulation of enzymes crucial for histone lactylation, including p300 and HDAC1, leads to reduced histone lactylation and accelerated cellular senescence. Consistently, the suppression of glycolysis and the depletion of histone lactylation are also observed during skeletal muscle aging. Modulating the enzymes also leads to the loss of histone lactylation in skeletal muscle, downregulating DNA repair and proteostasis pathways and accelerating muscle aging. Running exercise increases the levels of glycolysis and histone lactylation, thereby helping to preserve the proper function of skeletal muscle. Our study highlights the significant roles of histone lactylation in modulating cellular senescence and muscle aging, suggesting that this modification may serve as an innovative biomarker for senescence.
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