Genomic and transcriptomic analysis of Bovine P.multocida serogroup A strains reveals insights into virulence attenuation
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA756178 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR15524922_1.fastq.gz | Fastqsanger.gz | |||
| SRR15524922_2.fastq.gz | Fastqsanger.gz | |||
| SRR15524923_1.fastq.gz | Fastqsanger.gz | |||
| SRR15524923_2.fastq.gz | Fastqsanger.gz | |||
| SRR15524924_1.fastq.gz | Fastqsanger.gz |
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Project description:Pasteurella multocida is one of the main pathogens of bovine respiratory disease (BRD), which has brought great losses to the cattle industry. The Pm3 strain was a natural isolates, its pathogenic stronger and sensitive to fluoroquinolones. A highly fluoroquinolone resistant strain Pm64(MIC=64 μg/mL) was formed after continuous induction with subinhibitory concentration (1/2MIC) of enrofloxacin，with the enhanced growth characteristics and large attenuation of pathogenicity in mice. In this study, we report the whole genome sequence and the transcription profile by RNA-Seq of strain Pm3/Pm64. The results showed that there was not too much difference between the two strains at the genome level, 24 and 8 genes could be recognized were added and lost in the gene islands(GIs) of Pm64, Those gene involved in DNA binding, trehalose metabolism, material transportation, capsule synthesis, prophage, amino acid metabolism and other functions. 558 up-regulated and 568 down-regulated genes were found in Pm3 campared with Pm64, from which 20 virulence factor-related DEGs were screened. Genes differentially transcribed were mostly associated with capsular polysaccharide(CPS), lipopolysaccharide (LPS), lipooligosaccharide (LOS), Iron utilization and biofilm composition. We speculated that the main mechanism of virulence attenuation after the formation of resistance of Pm64 comes from the change of the expression profile of these genes. This report helps to elucidate the toxicity targets of P. multocida serogroup A and provide helps for the following research on pathogenesis and antimicrobial drugs development.
2021-08-21 | GSE182406 | GEO
Project description:The capsular serotype has long been associated with the virulence of Streptococcus pneumoniae. Here we present an in-depth study of phenotypic and genetic differences between serotype 3 and serogroup 11 S. pneumoniae clinical isolates from both the general and indigenous populations of Australia. Both serotypes/groups included clonally unrelated strains with differences in well-known polymorphic virulence genes, such as nanA and pspA, as demonstrated by multilocus sequence typing and Western blot analysis. Nonetheless, the serotype 3 strains were consistently and significantly more virulent in mice than the serogroup 11 strains. Despite extensive genomic analysis, noncapsular genes common to one serotype/group but not the other were not identified. Nevertheless, following the conversion of a serotype 11A isolate to serotype 3 and subsequent analysis in an intranasal infection model, it was evident that both capsular and noncapsular factors determine the virulence phenotype in mice. However, it appears that these noncapsular factors vary from strain to strain. Data is also available from http://bugs.sgul.ac.uk/E-BUGS-126
2011-12-01 | E-BUGS-126 | biostudies-arrayexpress
Project description:Pasteurella multocida is one of the primary pathogens of bovine respiratory disease (BRD), and causes huge losses in the cattle industry. The Pm3 strain was a natural isolate, which is a strong form of pathogen and is sensitive to fluoroquinolones antibiotics. A high fluoroquinolone resistant strain, Pm64 (MIC = 64 μg/mL), was formed after continuous induction with subinhibitory concentration (1/2 MIC) of enrofloxacin, with the enhanced growth characteristics and large attenuation of pathogenicity in mice. This study reports the whole genome sequence and the transcription profile by RNA-Seq of strain Pm3/Pm64. The results showed an ineffective difference between the two strains at the genome level. However, 32 genes could be recognized in the gene islands (GIs) of Pm64, in which 24 genes were added and 8 genes were lost. Those genes are involved in DNA binding, trehalose metabolism, material transportation, capsule synthesis, prophage, amino acid metabolism, and other functions. In Pm3 strain, 558 up-regulated and 568 down-regulated genes were found compared to Pm64 strain, from which 20 virulence factor-related differentially expressed genes (DEGs) were screened. Mainly differentially transcribed genes were associated with capsular polysaccharide (CPS), lipopolysaccharide (LPS), lipooligosaccharide (LOS). Iron utilization, and biofilm composition. We speculated that the main mechanism of virulence attenuation after the formation of resistance of Pm64 comes from the change of the expression profile of these genes. This report elucidated the toxicity targets of P. multocida serogroup A which provide fundamental information toward the understanding of the pathogenic mechanism and to decreasing antimicrobial drugs resistance.
| S-EPMC8631534 | biostudies-literature
Project description:Background: Members of E. coli serogroup O45 are porcine enteropathogenic E. coli (PEPEC) strains which cause post-weaning diarrhea and produce characteristic attaching and effacing (A/E) lesions. Most of O45 PEPEC strains possess the locus of enterocyte effacement (LEE), encoding the virulence factors for A/E lesions, and often possess the paa gene, which is thought to contribute to the early stages of PEPEC virulence. Methodology: Nine O45 PEPEC strains and a rabbit enteropathogenic (REPEC) strain, known to produce A/E lesions, were characterized using an E. coli O157-E. coli K12 whole genome microarray and a virulence gene-specific microarray, and by PCR experiments. Results: Based on their virulence genes profiles, the 10 strains were characterized as atypical EPEC. The differences in their genomes pointed to two distinct evolutionary groups of O45 PEPEC, Group I and Group II, and to the contribution these genetic differences have on virulence in pigs. Group I contained the REPEC strain and four O45 PEPEC strains known to induce severe A/E lesions in challenged pigs whereas Group II was composed of five other O45 PEPEC strains which induced less severe or no A/E lesions in challenged pigs. Significant differences between Groups I and II were found in the presence or absence of 50 O-Islands (OIs) or S-loops and 13 K-islands (KIs) or K-loops, including the virulence-associated islands OI#1 (S-loop#1), OI#47 (S-loop#71), OI#57 (S-loop#85), OI#71 (S-loop#108), OI#115, OI#122, and OI#154 (S-loop#253).
2009-07-11 | GSE17036 | GEO
Project description:In this study we compared the transcriptome of bovine macrophages infected with two Mycobacterium bovis strains of variable virulence, co-cultured with autologous lymphocytes. We used the highly virulent M. bovis strain called Mb04-303 and the attenuated Mb534 strain. We first observed that only the infection of bovine macrophages with the virulent strain, Mb04-303, induced in peripheral bovine mononuclear cells a powerful innate immune response capable of controlling the intracellular mycobacterial replication.By RNAseq analysis we found that infections with Mb04-303 downregulated the KEAP1-NFE2L2 pathway that encodes a transcriptional factor involved in antioxidant genes and inflammasome activation and upregulated the type 1 interferon signalling pathway, compared to the infections with the attenuated Mb534 strain. T
2023-09-14 | GSE241059 | GEO
Project description:Changing antigenic structure such as capsule polysaccharide is a common strategy for bacterial pathogen to evade host immune system. In this regard, the recent emergence of an invasive W:2a:P1.7-2,4 ST-11 strain in New Zealand, which is an uncommon pathogenic serogroup, was investigated for its genetic origins. Molecular typing of 103 meningococcal isolates with similar serotyping characteristics was undertaken to determine genetic relationships. Results indicated that the W:2a:P1.7-2,4 strain had emerged via capsule switching from an existing group C strain (C:2a:P1.7 2,4). Neither of the upstream and downstream sites of recombination could be elucidate but sequence analysis demonstrated that at least 45 kb of DNA was involved in the recombination event. This included the entire capsule gene cluster. Genomic DNA isolated from serogroup C strains (n=4) and serogroup W strains (n=4) were compared using Pan-neisseria DNA microarray.
2009-06-03 | E-MEXP-1910 | biostudies-arrayexpress
Project description:Background: Members of E. coli serogroup O45 are porcine enteropathogenic E. coli (PEPEC) strains which cause post-weaning diarrhea and produce characteristic attaching and effacing (A/E) lesions. Most of O45 PEPEC strains possess the locus of enterocyte effacement (LEE), encoding the virulence factors for A/E lesions, and often possess the paa gene, which is thought to contribute to the early stages of PEPEC virulence. Methodology: Nine O45 PEPEC strains and a rabbit enteropathogenic (REPEC) strain, known to produce A/E lesions, were characterized using an E. coli O157-E. coli K12 whole genome microarray and a virulence gene-specific microarray, and by PCR experiments. Results: Based on their virulence genes profiles, the 10 strains were characterized as atypical EPEC. The differences in their genomes pointed to two distinct evolutionary groups of O45 PEPEC, Group I and Group II, and to the contribution these genetic differences have on virulence in pigs. Group I contained the REPEC strain and four O45 PEPEC strains known to induce severe A/E lesions in challenged pigs whereas Group II was composed of five other O45 PEPEC strains which induced less severe or no A/E lesions in challenged pigs. Significant differences between Groups I and II were found in the presence or absence of 50 O-Islands (OIs) or S-loops and 13 K-islands (KIs) or K-loops, including the virulence-associated islands OI#1 (S-loop#1), OI#47 (S-loop#71), OI#57 (S-loop#85), OI#71 (S-loop#108), OI#115, OI#122, and OI#154 (S-loop#253). 10 samples, with two microarrays per sample. Each microarray includes duplicates of every spot.
2010-05-16 | E-GEOD-17036 | biostudies-arrayexpress
Project description:Attenuated virulence of M. tuberculosis in the bovine host
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Project description:These experiments were performed to show a serogroup conversion in Vibrio cholerae from O1 to O139. For this purpose, V. cholerae O1 WT = A1552 was grown on crab shell fragments to induce natural competence for transformation. Purified DNA (2 ug each) from strain VC73-orf6/7-Kan-A was added after 24h and the cells grown further for 24h. The VC73-orf6/7-Kan-A strain is a ATCC25873 derivative (both O37 serogroup) which harbors a Kanamycin cassette in the O37 region (as part of the operon between orf6 and orf7 w/o own promotor) for better selection. Transformants were selected on LB+Kan plates. Three clones were selected from each experiment and analyzed by microarray hybridization (BioPrime. Array CGH Genomic Labeling from Invitrogen). Two microarray replicates were done per clone. Comparison of A1552 versus VC73-orf6/7-Kan-A is shown as control. A genotyping experiment design type classifies an individual or group of individuals on the basis of alleles, haplotypes, SNP's. Keywords: genotyping_design
2007-04-26 | GSE5935 | GEO
Project description:These experiments were performed to show a serogroup conversion of Vibrio cholerae from O1 to O139. For this purpose, V. cholerae O1 El Tor (A1552) was grown on crab shell fragments to induce natural competence for transformation. Purified DNA (4 ug each) from strain MO10, an O139 serogroup strain, was added after 24h and the cells were further grown for 24h. After detachment from the crab shell fragments, bacteria were poured into soft-agar and overlaid onto LB plates. Mukerjee's El Tor phage V (a gift of Dr. M.S. Islam) was dropped onto the surface of the bacteria containing soft-agar. The plaques formed by killing non-transformed A1552 cells possessed resistant clones which were picked and further selected for opaque morphotype and agglutination by O139-specific antiserum. Four clones were selected from each independent experiment and analyzed by microarray hybridization (BioPrime. Array CGH Genomic Labeling from Invitrogen). Two microarray replicates were done per clone. Strain Names: ApO139#2 / ApO139#4 / ApO139#6 / ApO139#8 are four clones analyzed after the first experiment; AIIpO139#3 / AIIpO139#4 / AIIpO139#5 / AIIpO139#6 are four clones analyzed after the second independent experiment. Two MA replicates for each clone were done. CGHs of A1552 versus MO10 are provided as control. Keywords: array CGH
2007-04-25 | GSE5302 | GEO