Sequencing and functional annotation of avian pathogenic Escherichia coli serogroup O78 strains reveals the evolution of E. coli lineages pathogenic for poultry via distinct mechanisms

Avian pathogenic Escherichia coli (APEC) causes respiratory and systemic disease in poultry. Sequencing of a multilocus sequence type 95 (ST95) serogroup O1 strain previously indicated that APEC resembles E. coli causing extraintestinal human diseases. We sequenced the genomes of two strains of another dominant APEC lineage (ST23 serogroup O78 strains χ7122 and IMT2125) and compared them to each other and to the reannotated APEC O1 sequence. For comparison, we also sequenced a human enterotoxigenic E. coli (ETEC) strain of the same ST23 serogroup O78 lineage. Phylogenetic analysis indicated that the APEC O78 strains were more closely related to human ST23 ETEC than to APEC O1, indicating that separation of pathotypes on the basis of their extraintestinal or diarrheagenic nature is not supported by their phylogeny. The accessory genome of APEC ST23 strains exhibited limited conservation of APEC O1 genomic islands and a distinct repertoire of virulence-associated loci. In light of this diversity, we surveyed the phenotype of 2,185 signature-tagged transposon mutants of χ7122 following intra-air sac inoculation of turkeys. This procedure identified novel APEC ST23 genes that play strain- and tissue-specific roles during infection. For example, genes mediating group 4 capsule synthesis were required for the virulence of χ7122 and were conserved in IMT2125 but absent from APEC O1. Our data reveal the genetic diversity of E. coli strains adapted to cause the same avian disease and indicate that the core genome of the ST23 lineage serves as a chassis for the evolution of E. coli strains adapted to cause avian or human disease via acquisition of distinct virulence genes

Developmental changes in apolipoprotein B gene expression in the liver of fetal calves

International audienceChanges in apolipoprotein (apo B) gene expression in the liver were determined in fetal calves from 90 to 260 days of intrauterine life. Results were compared with those obtained from the livers of I-month-old calves and adult cows. By Western blot analysis using a rabbit antiserum to bovine apo B, apo B100 was detected from 90 days of intrauterine life. Apo B100 was shown to be the only form of apo B detected in the liver of fetal calves whatever the gestational age indicating the lack of editing process during the prenatal period. Hepatic apo B contents were stable during intrauterine life and comparable to those of calves and lower than those of cows. Hepatic contents of apo B mRNA. increased with the gestational age similarly to total RNA. Values of apo B mRNA at 260 days of intrauterine life were comparable to those in the liver of 1-month-old calves and adult cows. These results suggested that hepatic synthesis of calf apo B during fetal development is specifically regulated at a posttranscriptional level, either by a decrease in the rate of translation and/or by an increase in the rate of intracellular apo B degradation

Valeur nutritive des graines de soja crues ou extrudées pour les ruminants

National audienc