Comparative RNA-Seq based dissection of the regulatory networks and environmental stimuli underlying Vibrio parahaemolyticus gene expression during infection.
Bottom Line: Vibrio parahaemolyticus is the leading worldwide cause of seafood-associated gastroenteritis, yet little is known regarding its intraintestinal gene expression or physiology.Our analyses also suggest that V. parahaemolyticus has access to glucose or other preferred carbon sources in vivo, but that iron is inconsistently available.The V. parahaemolyticus transcriptional response to in vivo growth is far more widespread than and largely distinct from that of V. cholerae, likely due to the distinct ways in which these diarrheal pathogens interact with and modulate the environment in the small intestine.
Affiliation: The Broad Institute, Cambridge, MA, USA Division of Infectious Diseases, Department of Microbiology and Immunobiology, Brigham & Women's Hospital, Harvard Medical School and HHMI, 181 Longwood Ave., Boston, MA, USA email@example.com.Show MeSH
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Mentions: Our data indicate that ExsA is up-regulated in vivo (Supplementary Tables S1 and S2), and comparative analyses suggest that increased ExsA is responsible for up-regulation of numerous additional genes in vivo. The set of in vivo-induced genes includes a majority (50 of 70) genes previously reported to be induced by ExsA, including nine genes that are not in the T3SS1 gene cluster (Figure 5A, also Supplementary Table S5). Furthermore, although levels of ExsA transcripts are elevated in CF from all three rabbits, they are markedly less increased in CF3, in which T3SS1 up-regulation was not apparent. This is consistent with ExsA levels needing to reach a threshold to mediate downstream events; however, it is also possible that ExsA activity is dependent upon an additional (undefined) factor absent in bacteria in CF3. Levels of ExsA are thought to be responsive to increased calcium and to reduced iron levels (13), raising the possibility that intraintestinal variability in these ions accounts for at least some of the transcriptional heterogeneity we observed among the cecal fluid samples.
Affiliation: The Broad Institute, Cambridge, MA, USA Division of Infectious Diseases, Department of Microbiology and Immunobiology, Brigham & Women's Hospital, Harvard Medical School and HHMI, 181 Longwood Ave., Boston, MA, USA firstname.lastname@example.org.