In Silico Evaluation of Genes Orthologous to Genes Associated with Pathogenesis in Other Intracellular Bacteria

Overview

Journal Microorganisms

Specialty Microbiology

Date 2024 Aug 29

PMID 39203437

Authors

Mirtha E Suarez-Duarte

Renato L Santos

Carlos E R Pereira

Talita P Resende

Matheus D Araujo

Paula A Correia

Jessica C R Barbosa

Ricardo P Laub

Diego L N Rodrigues

Flavia F Aburjaile

Roberto M C Guedes

Affiliations

Soon will be listed here.

Abstract

Proliferative enteropathy is an enteric disease caused by the bacterium , which affects several species of domestic and wild animals. The mechanisms underlying the mechanisms employed by to cause host cell proliferation are poorly understood, mostly because this bacterium is extremely difficult to isolate and propagate in vitro. Comparative genomics methods for searching for genes orthologous to genes known to be associated with pathogenesis allow identification of genes potentially involved in pathogenesis by the pathogen of interest. The goal of this study was to carry out in silico research on genes orthologous to genes required for intracellular invasion and survival present in other pathogenic bacteria, particularly , , , , , subspecies , , , , and . A total of 127 genes associated with invasion and intracellular survival from five known intracellular bacteria were mapped against the predicted proteomes of all strains publicly available on GenBank, using the OrthoFinder program. A total of 45 genes were orthologous to genes associated with pathogenesis of other intracellular bacteria. Genes putatively associated with signal the transduction of chemotaxis and cell motility were identified. Genes related to DNA binding and repair were also identified, with some of them supporting a possible association of bacteria with macrophages or inducing pro-inflammatory responses. The homology-based identification of these genes suggests their potential involvement in the virulence and pathogenicity of , opening avenues for future research and insights into the molecular mechanisms of -elicited proliferative enteropathy.

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