bioRxiv Science⌕ Search

Biology subjects

Garcia Contreras, R.

Publications and source records attributed to Garcia Contreras, R..

2 recordsLinked to original sources

Resistome, Virulome, Mobilome, And Biosynthetic Gene Clusters Adaptations of Acinetobacter Baumannii Mexican Strains Across the Pre- and of the COVID-19 Period: Insights from Whole-Genome Sequencing

BackgroundAcinetobacter baumannii is a critical multidrug-resistant pathogen whose genomic landscape in Mexico has been reshaped by the COVID-19 pandemic. While global studies have highlighted distinctive sequence type distributions, systematic analyses in Mexico remain limited. MethodsWe analyzed 194 genomes, including 47 newly sequenced post-COVID isolates (MIQ), alongside 147 publicly available genomes (HPG). Whole-genome sequencing was combined with phylogenetic reconstruction, resistome and virulome profiling based on gene presence and absence, mobilome analysis, and biosynthetic gene cluster (BGC) characterization. ResultsTwo major clades dominated by Oxford STs 758, 208, 417, and 369 were identified. Resistome profiling uncovered 128 distinct resistome profiles (combinations of genes) and 44 emerging antimicrobial resistance genes (ARGs), with an increased number of resistance genes in the strains obtained during the pandemic. Virulome analysis revealed enrichment of metabolic adaptation genes (argG, carA, ilvC) in MIQ strains. Mobilome profiling demonstrated enrichment of ISAbA1 and ISAbA3 elements, known to mobilize carbapenemase genes. BGC analysis showed conserved siderophores involved in virulence, alongside diversification of the secondary metabolite repertoires in MIQ genomes. Additional observations included geographic mixing of clades across Jalisco, Aguascalientes, and Mexico City and referral bias toward carbapenemase-positive isolates. ConclusionThe genomic landscape of A. baumannii in Mexico has diversified post-COVID, with evidence of inter-regional transmission, referral bias, virulome expansion, mobilome-driven ARG dissemination, and metabolic adaptation. These findings underscore the urgent need for coordinated genomic surveillance, functional and clinical validation of adaptation signals, and regionally integrated infection control strategies to mitigate resistance trajectories. Graphical abstractIntegrative genomic profiling of A. baumannii isolates from Mexico. Workflow summarizing the analysis of 194 genomes (147 historic public genomes, 47 novel MIQ strains). Clinical isolates were identified by MALDI Biotyper and tested with BD Phoenix M50. Whole genome sequencing enabled phylogenetic and MLST analyses, resistome and virulome profiling, mobilome characterization, and BGC identification using BIGSCAPE and antiSMASH. Outputs include phylogenetic clustering, resistance/virulence gene distributions, and biosynthetic potential across Mexican regions. O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=84 SRC="FIGDIR/small/712163v1_ufig1.gif" ALT="Figure 1"> View larger version (27K): org.highwire.dtl.DTLVardef@74c87borg.highwire.dtl.DTLVardef@1160aa7org.highwire.dtl.DTLVardef@1564c1org.highwire.dtl.DTLVardef@89e91b_HPS_FORMAT_FIGEXP M_FIG C_FIG

microbiology↗

Serine Recombinase PinR Inverts Cryptic Prophage DNA to Block Adsorption of Phages

Recombinases catalyze site-specific integration, excision, and inversion of DNA and are found in myriad defense islands; however, their function in phage-defense is unknown as they are frequently dismissed as markers of prophages. Here, we characterize the physiological role of the previously-uncharacterized serine recombinase PinR of Escherichia coli cryptic prophage rac and discover that it inhibits T2 phage infection by inverting a 1,797 bp segment in a different cryptic prophage e14 to inhibit T2 infection; this inversion leads to the formation of a novel protein from two spliced genes, StfE2, that we find blocks phage adsorption. Modeling shows StfE2 inhibits T2 phage adsorption by preventing Gp38 binding to its primary receptors porins FadL and OmpF. Corroborating the receptor-blocking hypothesis, T2 escape mutants evolve resistance to PinR phage defense by mutating gp38 to remove 16 aa in the hyper variable region 3. Therefore, we discovered the first recombinase-activated phage inhibition system.

molecular biology↗