Similar Datasets
Project description:Plant response to pathogen infection varies within a leaf, yet this heterogeneity is not well resolved. We exposed Arabidopsis to Pseudomonas syringae or mock treatment and profiled the transcriptomes of 11,000 individual cells using single-cell RNA sequencing. Integrative analysis of cell populations from Pseudomonas and mock inoculated leaves identified five distinct pathogen responsive cell clusters exhibiting transcriptional responses ranging from immunity to susceptibility. Pseudotime analyses through pathogen infection revealed a continuum of disease progression from an immune to susceptible state. Confocal imaging of promoter reporter lines for pathogen responsive cell clusters visualized immune activated cell clusters surrounding substomatal cavities colonized by bacteria, suggesting immune clusters are sites of early pathogen invasion. Susceptibility cell clusters exhibited more general localization and were highly induced at later stages of infection. Overall, our work uncovers cellular heterogeneity within an infected leaf and provides unique insight into plant differential response to infection at a single-cell level.
2022-10-07 | GSE213622 | GEO
Project description:Plant response to pathogen infection varies within a leaf, yet this heterogeneity is not well resolved. We exposed Arabidopsis to Pseudomonas syringae or mock treatment and profiled the transcriptomes of 11,000 individual cells using single-cell RNA sequencing. Integrative analysis of cell populations from Pseudomonas and mock inoculated leaves identified five distinct pathogen responsive cell clusters exhibiting transcriptional responses ranging from immunity to susceptibility. Pseudotime analyses through pathogen infection revealed a continuum of disease progression from an immune to susceptible state. Confocal imaging of promoter reporter lines for pathogen responsive cell clusters visualized immune activated cell clusters surrounding substomatal cavities colonized by bacteria, suggesting immune clusters are sites of early pathogen invasion. Susceptibility cell clusters exhibited more general localization and were highly induced at later stages of infection. Overall, our work uncovers cellular heterogeneity within an infected leaf and provides unique insight into plant differential response to infection at a single-cell level.
2022-10-07 | GSE213616 | GEO
Project description:Plant response to pathogen infection varies within a leaf, yet this heterogeneity is not well resolved. We expose Arabidopsis to Pseudomonas syringae or mock treatment and profile >11,000 individual cells using single-cell RNA sequencing. Integrative analysis of cell populations from both treatments identifies distinct pathogen-responsive cell clusters exhibiting transcriptional responses ranging from immunity to susceptibility. Pseudotime analyses through pathogen infection reveals a continuum of disease progression from an immune to a susceptible state. Confocal imaging of promoter-reporter lines for transcripts enriched in immune cell clusters shows expression surrounding substomatal cavities colonized or in close proximity to bacterial colonies, suggesting that cells within immune clusters represent sites of early pathogen invasion. Susceptibility clusters exhibit more general localization and are highly induced at later stages of infection. Overall, our work shows cellular heterogeneity within an infected leaf and provides insight into plant differential response to infection at a single-cell level.
| S-EPMC10528479 | biostudies-literature
Project description:Single-cell profiling of complex plant responses to Pseudomonas syringae infection
| PRJNA881947 | ENA
Project description:We used three different strains of Pseudomonas syringae pv tomato DC3000 to investigate systemic responses to infection in Arabidopsis and the development of SAR. Wildtype DC3000, the hrpA mutant and DC3000 carrying the avirulence gene avrRpm1 were syringe infiltrated into 4-week-old plants at a concentration of 10e8 cfu/ml. At least 5 leaves per plant were infiltrated and at least 10 plants were pooled for each sample. Systemic, uninfected tissue was then harvested at 8, 12 and 21h after inoculation. Three independent experiments were carried out to give three biological replicates for each timepoint.
2009-12-10 | GSE19264 | GEO
Project description:Single-cell profiling of complex plant responses to Pseudomonas syringae infection [scRNA-seq]
| PRJNA881949 | ENA
Project description:We used three different strains of Pseudomonas syringae pv tomato DC3000 to investigate systemic responses to infection in Arabidopsis and the development of SAR. Wildtype DC3000, the hrpA mutant and DC3000 carrying the avirulence gene avrRpm1 were syringe infiltrated into 4-week-old plants at a concentration of 10e8 cfu/ml. At least 5 leaves per plant were infiltrated and at least 10 plants were pooled for each sample. Systemic, uninfected tissue was then harvested at 8, 12 and 21h after inoculation. Three independent experiments were carried out to give three biological replicates for each timepoint. 27 samples were used in this experiment.
2009-12-09 | E-GEOD-19264 | biostudies-arrayexpress
Project description:Single-cell profiling of complex plant responses to Pseudomonas syringae infection [bulk RNA-seq]
| PRJNA881937 | ENA
Project description:The circadian clock drives daily rhythms of many plant physiological responses, providing a competitive advantage that improves plant fitness and survival rates [1-5]. Whereas multiple environmental cues are predicted to regulate the plant clock function, most studies focused on understanding the effects of light and temperature [5-8]. Increasing evidence indicates a significant role of plant-pathogen interactions on clock regulation [9, 10], but the underlying mechanisms remain elusive. In Arabidopsis, the clock function largely relies on a transcriptional feedback loop between morning (CCA1 and LHY)- and evening (TOC1)-expressed transcription factors [6-8]. Here, we focused on these core components to investigate the Arabidopsis clock regulation using a unique biotic stress approach. We found that a single-leaf Pseudomonas syringae infection systemically lengthened the period and reduced the amplitude of circadian rhythms in distal uninfected tissues. Remarkably, the low-amplitude phenotype observed upon infection was recapitulated by a transient treatment with the defense-related phytohormone salicylic acid (SA), which also triggered a significant clock phase delay. Strikingly, despite SA-modulated circadian rhythms, we revealed that the master regulator of SA signaling, NPR1 [11, 12], antagonized clock responses triggered by both SA treatment and P. syringae. In contrast, we uncovered that the NADPH oxidase RBOHD [13] largely mediated the aforementioned clock responses after either SA treatment or the bacterial infection. Altogether, we demonstrated novel and unexpected roles for SA, NPR1, and redox signaling in clock regulation by P. syringae and revealed a previously unrecognized layer of systemic clock regulation by locally perceived environmental cues.
| S-EPMC5820129 | biostudies-literature
Project description:The bacterial plant pathogen Pseudomonas syringae deploys a type III secretion system (T3SS) to deliver effector proteins into plant cells to facilitate infection, for which many effectors have been characterized for their interactions. However, few T3SS Hrp (hypersensitive response and pathogenicity) proteins from the T3SS secretion apparatus have been studied for their direct interactions with plants. Here, we show that the P. syringae pv. tomato DC3000 T3SS protein HrpP induces host cell death, suppresses pattern-triggered immunity (PTI), and restores the effector translocation ability of the hrpP mutant. The hrpP-transgenic Arabidopsis lines exhibited decreased PTI responses to flg22 and elf18 and enhanced disease susceptibility to P. syringae pv. tomato DC3000. Transcriptome analysis reveals that HrpP sensing activates salicylic acid (SA) signaling while suppressing jasmonic acid (JA) signaling, which correlates with increased SA accumulation and decreased JA biosynthesis. Both yeast two-hybrid and bimolecular fluorescence complementation assays show that HrpP interacts with mitogen-activated protein kinase kinase 2 (MKK2) on the plant membrane and in the nucleus. The HrpP truncation HrpP1-119, rather than HrpP1-101, retains the ability to interact with MKK2 and suppress PTI in plants. In contrast, HrpP1-101 continues to cause cell death and electrolyte leakage. MKK2 silencing compromises SA signaling but has no effect on cell death caused by HrpP. Overall, our work highlights that the P. syringae T3SS protein HrpP facilitates effector translocation and manipulates plant immunity to facilitate bacterial infection. IMPORTANCE The T3SS is required for the virulence of many Gram-negative bacterial pathogens of plants and animals. This study focuses on the sensing and function of the T3SS protein HrpP during plant interactions. Our findings show that HrpP and its N-terminal truncation HrpP1-119 can interact with MKK2, promote effector translocation, and manipulate plant immunity to facilitate bacterial infection, highlighting the P. syringae T3SS component involved in the fine-tuning of plant immunity.
| S-EPMC10269811 | biostudies-literature