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ABSTRACT:
PROVIDER: PRJNA542580 | ENA |
REPOSITORIES: ENA
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Project description:Erythromycin/tetracycline resistant strain
| PRJNA32925 | ENA
Project description:Erythromycin is the drug of choice to treat campylobacteriosis, but resistance to this antibiotic is rising. The adaptive mechanisms employed by Campylobacter jejuni to erythromycin treatment remain unknown. The aim of this study is to determine the molecular basis underlying CampylobacterM-bM-^@M-^Ys immediate response to Ery treatment. The design utilized an available two color microarray slide for the entire transcriptome of Campylobacter jejuni macrolide resistant strain JL272. One hybridizations were performed: sham-treated JL272 v.s. lethal dose erythromycin treated JL272. Samples were independently grown and harvested. There were three biological replicates of each sample.
2013-10-10 | E-GEOD-43025 | biostudies-arrayexpress
Project description:Vancomycin/erythromycin resistant clinical isolate
| PRJNA32937 | ENA
Project description:Methicillin-resistant Staphylococcus aureus (MRSA) remains a global health threat with an over 14% fatality rate, in case of invasive infection, in 2011. Multi-drug resistance is the main reason for the failure of therapy. Use of antimicrobial drug combinations with synergistic effect is increasingly seen as a critical strategy to combat multi-drug resistant pathogens such as MRSA. However, the mechanism of synergistic effect has yet been systematically studied. In this work, we investigated a new erythromycin derivative, SIPI-8294, which has been demonstrated to have synergistic effect with oxacillin against MRSA, unlike its parent compound erythromycin. To obtain insights into the mechanism for the synergistic effect, label-free quantitative proteomics was employed. Cultured MRSA was exposed to sub-inhibitory doses of oxacillin, SIPI-8294, erythromycin, and combinations of SIPI-8294/oxacillin and erythromycin/oxacillin to reveal the global proteome responses to drug treatment. Results showed that 200 proteins were differentially expressed in SIPI-8294/oxacillin-treated cells. Among these proteins, the expression levels of penicillin binding protein 2a and β-lactamase, two proteins mainly responsible for oxacillin resistance, were four times lower in the SIPI-8294/oxacillin treatment group than in the erythromycin/oxacillin treatment group. Quantitative real-time PCR analysis also revealed similar trends at the transcription level. These results suggest that the synergistic mechanism may be related to interference with the known oxacillin resistance mechanism. The data also provided some evidence that the combination of SIPI-8294 and oxacillin appears to impact oxidation-reduction homeostasis and cell wall biosynthesis.
2022-03-01 | PXD001494 | Pride
Project description:In this study we have used the rifampicin selection as a tool to genetically improve the erythromycin producer Saccharopolyspora erythraea. Two rifampicin-resistant (rif) mutants, rif1 and rif6, have been characterized in more detail. With respect to the parental strain NRRL2338, rif1 (harboring the missense S444F) exhibited higher respiratory performance and final erythromycin yields; in contrast, rif6 (harboring the missense Q426R) was slow-growing, developmental-defective and severely impaired in erythromycin production. The results of genome-wide analysis of expression profiles using DNA micro-arrays demonstrated that these mutations deeply changed the transcriptional profile of S. erythraea with marked regional distribution. Keywords: mutants versus wild type comparison in a time course experiment
2009-04-12 | GSE12017 | GEO
Project description:In this study we have used the rifampicin selection as a tool to genetically improve the erythromycin producer Saccharopolyspora erythraea. Two rifampicin-resistant (rif) mutants, rif1 and rif6, have been characterized in more detail. With respect to the parental strain NRRL2338, rif1 (harboring the missense S444F) exhibited higher respiratory performance and final erythromycin yields; in contrast, rif6 (harboring the missense Q426R) was slow-growing, developmental-defective and severely impaired in erythromycin production. The results of genome-wide analysis of expression profiles using DNA micro-arrays demonstrated that these mutations deeply changed the transcriptional profile of S. erythraea with marked regional distribution. Keywords: mutants versus wild type comparison in a time course experiment Total of 12 Samples
2009-04-12 | E-GEOD-12017 | biostudies-arrayexpress
Project description:Microarray was used to analyze azole resistance of Candida glabrata oropharyngeal isolates from 7 hematopoietic stem cell transplant recipients receiving fluconazole prophylaxis. Transcriptional profiling of the sequential-paired clinical isolates by microarray revealed 19 genes upregulated in the majority of resistant isolates compared to their paired-susceptible isolates. All seven resistant isolates had greater than two fold upregulation of CgPDR1, a master transcriptional regulator of PDR network, and all 7 resistant isolates showed upregulation of known CgPDR1-target genes. The altered transcriptome can be explained in part by the observation that all 7 resistant isolates had acquired a single nonsynonymous mutation in their CgPDR1 ORF. Four mutations occurred in the regulatory domain (L280P, L344S, G348A, S391L) and one in the activation domain (G943S) while two mutations (N764I, R772I) occurred in an undefined region. Association of azole resistance and the CgPDR1 mutations was investigated in the same genetic background by introducing the CgPDR1 sequences from one sensitive and five resistant isolates into a laboratory azole-sensitive strain (cgpdr1) via integrative transformation. The cgpdr1 strain was restored to wild-type fluconazole susceptibility when transformed with CgPDR1 from the susceptible isolate but became resistant when transformed with CgPDR1 from the resistant isolates. However, despite the identical genetic background, upregulation of CgPDR1 and CgPDR1-target genes varied between the 5 transformants, independent of the domain locations in which the mutations occurred. In sum, gain-of-function mutations in CgPDR1 not only contributed to the clinical azole resistance but different mutations had varying degrees of impact on the CgPDR1-target genes.
2010-07-07 | GSE21352 | GEO
Project description:Microarray was used to analyze azole resistance of Candida glabrata oropharyngeal isolates from 7 hematopoietic stem cell transplant recipients receiving fluconazole prophylaxis. Transcriptional profiling of the sequential-paired clinical isolates by microarray revealed 19 genes upregulated in the majority of resistant isolates compared to their paired-susceptible isolates. All seven resistant isolates had greater than two fold upregulation of CgPDR1, a master transcriptional regulator of PDR network, and all 7 resistant isolates showed upregulation of known CgPDR1-target genes. The altered transcriptome can be explained in part by the observation that all 7 resistant isolates had acquired a single nonsynonymous mutation in their CgPDR1 ORF. Four mutations occurred in the regulatory domain (L280P, L344S, G348A, S391L) and one in the activation domain (G943S) while two mutations (N764I, R772I) occurred in an undefined region. Association of azole resistance and the CgPDR1 mutations was investigated in the same genetic background by introducing the CgPDR1 sequences from one sensitive and five resistant isolates into a laboratory azole-sensitive strain (cgpdr1) via integrative transformation. The cgpdr1 strain was restored to wild-type fluconazole susceptibility when transformed with CgPDR1 from the susceptible isolate but became resistant when transformed with CgPDR1 from the resistant isolates. However, despite the identical genetic background, upregulation of CgPDR1 and CgPDR1-target genes varied between the 5 transformants, independent of the domain locations in which the mutations occurred. In sum, gain-of-function mutations in CgPDR1 not only contributed to the clinical azole resistance but different mutations had varying degrees of impact on the CgPDR1-target genes.
2010-07-07 | GSE21355 | GEO
Project description:Recently the membrane vesicles (MVs) production has been observed in Gram-positive bacterium, Cutibacterium acnes (C. acnes). In order to explore the mechanism of antibiotic resistance and the virulent components within the C. acnes-derived MVs, we isolated MVs from the clinical C. acnes, which were sensitive or resistant to antibiotics erythromycin and clindamycin. With the LC-MS/MS method, we detected several lipases, virulent factors and cell division protein differentially expressed between the sensitive and the resistant C. acnes-derived MVs.
2022-05-20 | PXD025460 | Pride
Project description:Comparative analysis of genome wide binding profile of Ncb2 in azole sensitive (AS, Gu4) and azole resistant (AR, Gu5) clinical isolates of Candida albicans. The goal was to study the role of Ncb2 in acquisition of drug resistance by comparing the binding profiles of Ncb2 in both the isolates.
2017-08-01 | GSE76858 | GEO