Holliday junction resolvase RuvC targets biofilm eDNA to facilitate pathogen spread in plants
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1128091 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR29545664_1.fastq.gz | Fastqsanger.gz | |||
| SRR29545664_2.fastq.gz | Fastqsanger.gz | |||
| SRR29545665_1.fastq.gz | Fastqsanger.gz | |||
| SRR29545665_2.fastq.gz | Fastqsanger.gz | |||
| SRR29545666_1.fastq.gz | Fastqsanger.gz |
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Project description:Biofilm lifestyle is critical for bacterial pathogens to colonize and protect themselves from host immunity and antimicrobial chemicals in plants and animals. The formation and regulation mechanism of phytobacterial biofilm are still obscure. Here, we found that Ralstonia solanacearum Resistance to ultraviolet C (RuvC) is highly abundant in biofilm and positively regulates pathogenicity by governing systemic movement in tomato xylem. RuvC protein accumulates at the later stage of biofilm and specifically targets the Holliday junction (HJ) like structures to disrupt biofilm extracellular DNA (eDNA) lattice, thus facilitating biofilm dispersal. Recombinant RuvC protein can resolve extracellular HJ prevent bacterial biofilm formation. Heterologous expression of R. solanacearum or Xanthomonas oryzae pv. oryzae RuvC with plant secretion signal in tomato or rice confers resistance to bacterial wilt or bacterial blight disease, respectively. Plant chloroplast localized HJ resolvase monokaryotic chloroplast 1 (MOC1) which is structural similar to bacterial RuvC shows a strong inhibit effect on bacterial biofilm formation. Re-localization of SlMOC1 to apoplast in tomato roots leads to increase resistance to bacterial wilt. Our novel finding reveals a critical pathogenesis mechanism of R. solanacearum and provides an efficient biotechnology strategy to improve plant resistance to bacteria vascular disease.
2024-09-29 | GSE270737 | GEO
Project description:In Staphylococcus aureus, the role of the GGDEF domain containing protein GdpS remains poorly understood. Previous studies reported that gdpS mutant strains had decreased biofilm formation due to changes in icaADBC expression that were independent of cyclic-di-GMP levels. We deleted gdpS in three unrelated S. aureus isolates, and analyzed the resultant mutants for alterations in biofilm formation, metabolism and transcription. Dynamic imaging during biofilm development showed that GdpS inhibited early biofilm formation in only two out of the three strains examined, without affecting bacterial survival. However, quantification of biofilm formation using crystal violet staining revealed that inactivation of gdpS affected biofilm formation in all three studied strains. Extraction of metabolites from S. aureus cells confirmed the absence of cyclic-di-GMP, suggesting that biofilm formation in this species differs from that in other Gram-positive organisms. In addition, targeted mutagenesis demonstrated that the GGDEF domain was not required for GdpS activity. Transcriptomic analysis revealed that the vast majority of GGDEF-regulated genes were involved in virulence, metabolism, cell wall biogenesis and eDNA release. Finally, expression of lrgAB or deletion of cidABC in a strain lacking gdpS confirmed the role of GdpS on regulation of eDNA production that occurred without an increase in cell autolysis. In summary, S. aureus GdpS contributes to cell-to-cell interactions during early biofilm formation by influencing expression of lrgAB and cidABC mediated eDNA release. We conclude that GdpS acts as a negative regulator of eDNA release.
2014-06-30 | GSE48656 | GEO
Project description:We studied how leukemia-associated mutations subvert normal adult hematopoiesis by genetically inducing them in specifically in murine hematopoietic stem cells (HSC) followed by lineage tracing in native hosts. Leukemia-initiating mutations such as Tet2 or Dnmt3a deletions did not increase the net HSC contribution in the steady state, whereasTet2 deletion slightly accelerated HSC contribution to myeloid lineages following microbial stimulation. In contrast, the leukemia-transforming KrasG12D mutation dramatically accelerated the contribution of mutant HSC to all hematopoietic lineages, rapidly creating a pre-leukemic state. The acceleration was mediated by KrasG12D-carrying multipotent progenitors (MPP) that rapidly outcompeted normal MPP and showed increased proliferation but lacked self-renewal capacity. In addition, mutant progenitor cells expressed the secreted stem/progenitor regulator osteopontin and showed enhanced CXCR4-dependent motility, both of which contributed to the accelerated spread of the mutation to mature cells. Thus, transforming mutations may facilitate their spread from HSC to mature cells via hypercompetitive progenitors, creating a two-component stem/progenitor circuit that underlies leukemogenesis.
2025-02-19 | GSE261879 | GEO
Project description:In Staphylococcus aureus, the role of the GGDEF domain containing protein GdpS remains poorly understood. Previous studies reported that gdpS mutant strains had decreased biofilm formation due to changes in icaADBC expression that were independent of cyclic-di-GMP levels. We deleted gdpS in three unrelated S. aureus isolates, and analyzed the resultant mutants for alterations in biofilm formation, metabolism and transcription. Dynamic imaging during biofilm development showed that GdpS inhibited early biofilm formation in only two out of the three strains examined, without affecting bacterial survival. However, quantification of biofilm formation using crystal violet staining revealed that inactivation of gdpS affected biofilm formation in all three studied strains. Extraction of metabolites from S. aureus cells confirmed the absence of cyclic-di-GMP, suggesting that biofilm formation in this species differs from that in other Gram-positive organisms. In addition, targeted mutagenesis demonstrated that the GGDEF domain was not required for GdpS activity. Transcriptomic analysis revealed that the vast majority of GGDEF-regulated genes were involved in virulence, metabolism, cell wall biogenesis and eDNA release. Finally, expression of lrgAB or deletion of cidABC in a strain lacking gdpS confirmed the role of GdpS on regulation of eDNA production that occurred without an increase in cell autolysis. In summary, S. aureus GdpS contributes to cell-to-cell interactions during early biofilm formation by influencing expression of lrgAB and cidABC mediated eDNA release. We conclude that GdpS acts as a negative regulator of eDNA release. Three strains UAMS-1, SA113 and SA564 were used in this study to compare wt with gdpS mutant after 5 hours of growth in static conditions (biofilm formation).
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Project description:Leukemogenic Kras mutation reprograms multipotent progenitors to facilitate its spread through the hematopoietic system
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