Expression of Adhesive Pili and the Collagen-Binding Adhesin Ace Is Activated by ArgR Family Transcription Factors in Enterococcus faecalis.
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ABSTRACT:
PROVIDER: PRJNA449531 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR6978910_1.fastq.gz | Fastqsanger.gz | |||
| SRR6978910_2.fastq.gz | Fastqsanger.gz | |||
| SRR6978911_1.fastq.gz | Fastqsanger.gz | |||
| SRR6978911_2.fastq.gz | Fastqsanger.gz | |||
| SRR6978912_1.fastq.gz | Fastqsanger.gz |
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Project description:In E. faecalis OG1RF, disruption of the ahrC gene encoding a predicted ArgR family transcription factor results in a severe defect in biofilm formation in vitro, as well as significant attenuation of virulence in multiple experimental infection models. Using RNA-seq, we observed ahrC-dependent changes in expression of over 20 genes. AhrC-repressed genes included predicted determinants of arginine catabolism and several other metabolic genes and predicted transporters, while AhrC-activated genes included determinants involved in production of surface protein adhesins. Most notably, the structural and regulatory genes of the ebp locus encoding adhesive pili were positively regulated, as well as the ace gene, encoding a collagen binding adhesin. Using lacZ transcription reporter fusions, we determined that ahrC and a second argR transcription factor gene, argR2, both function to activate expression of ebpR, which directly activates transcription of the pilus structural genes. Our data suggest that in wild-type E. faecalis, the low levels of EbpR limit expression of pili, and that biofilm biomass is also limited by the amount of pili expressed by the bacteria. Expression of ace is similarly activated by AhrC and ArgR2, but ace expression is not dependent on EbpR. Our results demonstrate the existence of novel regulatory cascades controlled by a pair of ArgR family transcription factors that may function as a heteromeric protein complex.
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Project description:It was shown previously that the disruption of the ahrC gene encoding a predicted ArgR family transcription factor results in a severe defect in biofilm formation in vitro, as well as a significant attenuation of virulence of Enterococcus faecalis strain OG1RF in multiple experimental infection models. Using transcriptome sequencing (RNA-seq), we observed ahrC-dependent changes in the expression of more than 20 genes. AhrC-repressed genes included predicted determinants of arginine catabolism and several other metabolic genes and predicted transporters, while AhrC-activated genes included determinants involved in the production of surface protein adhesins. Most notably, the structural and regulatory genes of the ebp locus encoding adhesive pili were positively regulated, as well as the ace gene, encoding a collagen-binding adhesin. Using lacZ transcription reporter fusions, we determined that ahrC and a second argR transcription factor gene, argR2, both function to activate the expression of ebpR, which directly activates the transcription of the pilus structural genes. Our data suggest that in the wild-type E. faecalis, the low levels of EbpR limit the expression of pili and that biofilm biomass is also limited by the amount of pili expressed by the bacteria. The expression of ace is similarly enhanced by AhrC and ArgR2, but ace expression is not dependent on EbpR. Our results demonstrate the existence of novel regulatory cascades controlled by a pair of ArgR family transcription factors that might function as a heteromeric protein complex.IMPORTANCE Cell surface adhesins play critical roles in the formation of biofilms, host colonization, and the pathogenesis of opportunistic infections by Enterococcus faecalis Here, we present new results showing that the expression of two major enterococcal surface adhesins, ebp pili, and the collagen-binding protein Ace is positively regulated at the transcription level by two argR family transcription factors, AhrC and ArgR2. In the case of pili, the direct target of regulation is the ebpR gene, previously shown to activate the transcription of the pilus structural genes, while the activation of ace transcription appears to be directly impacted by the two ArgR proteins. These transcription factors may represent new targets for blocking enterococcal infections.
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Project description:The goal of the current study was to characterize the cardiac transcriptional signature of the metabolic syndrome (MetS) murine model relative to the healthy, control heart and the differential changes induced by ACE-inhibition, a frequent intervention in MetS subjects, at the transcriptomic level in control and MetS hearts. Methods - LDLR-/-;ob/ob (DKO, MetS model) and C57Bl6/J (WT) mice were injected with ACE-inhibitor captopril (10 mg/kg/day) between 12 and 24 weeks of age, or NaCl 0,9% as controls. Transcriptome analysis (RNA-seq) from the whole heart RNA samples was performed. Differential gene expression was analysed with Cufdiff. Ingenuity Pathway Analysis (IPA) was used to determine functional enrichment, and analyse pathways, networks, and upstream regulators. Transcription factor motif enrichment analysis was performed with i-cisTarget. Results – 288 genes implicating 72 pathways were differentially expressed between DKO and WT hearts. The hallmarks of MetS in the heart were an increase in activity of the following pathways: ILK, Rho, dendritic cell maturation, production of nitric oxide and reactive oxygen species in macrophages, atherosclerosis, LXR-RXR, cardiac hypertrophy, and acute phase response. ACE-inhibition resulted in a limited transcriptional effect in WT hearts and in a decrease in activity of Rho-associated signalling pathways. In contrast, a more prominent transcriptional effect was observed in DKO hearts. Similar to WT, Rho-associated pathways were affected, but ACE-inhibition further displayed a counteracting effect on the pathways affected by MetS in the heart Conclusion –MetS and control mouse hearts have unique transcriptional profiles, with characteristic baseline gene expression landscapes prior to ACE-inhibition, and a partially specific transcriptional response to ACE-inhibition. The Rho-associated signalling pathways and Rho, Rock, Myl, and Fos genes represent potential therapeutic targets.
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Project description:Extracellular senile plaques of amyloid beta (Abeta) are a pathological hallmark in brain of patients with Alzheimer`s Disease (AD). Abeta is generated by the amyloidogenic processing of the amyloid precursor protein (APP). Concomitant to Abeta load, AD brain is characterized by an increase in protein level and activity of the angiotensin-converting enzyme (ACE). ACE inhibitors are a widely used class of drugs with established benefits for patients with cardiovascular disease. However, the role of ACE and ACE inhibition in the development of Abeta plaques and the process of AD-related neurodegeneration is not clear since ACE was reported to degrade Abeta. To investigate the effect of ACE inhibition on AD-related pathomechanisms, we used Tg2576 mice with neuron-specific expression of APPSwe as AD model. From 12 months of age, substantial Abeta plaque load accumulates in the hippocampus of Tg2576 mice as a brain region, which is highly vulnerable to AD-related neurodegeneration. The effect of central ACE inhibition was studied by treatment of 12 month-old Tg2576 mice for six months with the brain penetrating ACE inhibitor captopril. At an age of 18 months, hippocampal gene expression profiling was performed of captopril-treated Tg2576 mice relative to untreated 18 month-old Tg2576 controls with high Abeta plaque load. As an additional control, we used 12 month-old Tg2576 mice with low Abeta plaque load. Whole genome microarray gene expression profiling revealed gene expression changes induced by the brain-penetrating ACE inhibitor captopril, which could reflect the neuro-regenerative potential of central ACE inhibition. Microarray gene expression profiling was performed of hippocampi isolated from aged, 18 month-old Tg2576 (APPSwe-transgenic) AD mice with high Abeta plaque load relative to age-matched Tg2576 mice, which were treated for 6 months with the centrally active ACE inhibitor captopril. Another study group consisted of 12 month-old Tg2576 mice with low Abeta plaque load. In total, three study groups were analyzed, i.e. (i) 18 month-old untreated Tg2576 mice with high Abeta plaque load, (ii) age-matched Tg2576 mice treated for 6 months with the brain-penetrating ACE inhibitor captopril (20 mg/kg body weight/day in drinking water), and (iii) untreated 12 month-old Tg2576 mice with low Abeta plaque load reflecting the time point when captopril treatment was initiated. Two biological replicates were made of each group, and total hippocampal RNA of four mice was pooled for one gene chip.
2013-05-14 | E-GEOD-46871 | biostudies-arrayexpress