AUTHOR=White Corin V. , Herman Michael A. 

TITLE=Transcriptomic, Functional, and Network Analyses Reveal Novel Genes Involved in the Interaction Between Caenorhabditis elegans and Stenotrophomonas maltophilia

JOURNAL=Frontiers in Cellular and Infection Microbiology

VOLUME=8

YEAR=2018

URL=https://www.frontiersin.org/journals/cellular-and-infection-microbiology/articles/10.3389/fcimb.2018.00266

DOI=10.3389/fcimb.2018.00266

ISSN=2235-2988

ABSTRACT=<p>The bacterivorous nematode <italic>Caenorhabditis elegans</italic> is an excellent model for the study of innate immune responses to a variety of bacterial pathogens, including the emerging nosocomial bacterial pathogen <italic>Stenotrophomonas maltophilia</italic>. The study of this interaction has ecological and medical relevance as <italic>S. maltophilia</italic> is found in association with <italic>C. elegans</italic> and other nematodes in the wild and is an emerging opportunistic bacterial pathogen. We identified 393 genes that were differentially expressed when exposed to virulent and avirulent strains of <italic>S. maltophilia</italic> and an avirulent strain of <italic>E. coli</italic>. We then used a probabilistic functional gene network model (WormNet) to determine that 118 of the 393 differentially expressed genes formed an interacting network and identified a set of highly connected genes with eight or more predicted interactions. We hypothesized that these highly connected genes might play an important role in the defense against <italic>S. maltophila</italic> and found that mutations of six of seven highly connected genes have a significant effect on nematode survival in response to these bacteria. Of these genes, C48B4.1, <italic>mpk-2, cpr-4, clec-67</italic>, and <italic>lys-6</italic> are needed for combating the virulent <italic>S. maltophilia</italic> JCMS strain, while <italic>dod-22</italic> was solely involved in response to the avirulent <italic>S. maltophilia</italic> K279a strain. We further found that <italic>dod-22</italic> and <italic>clec-67</italic> were up regulated in response to JCMS vs. K279a, while C48B4.1, <italic>mpk-2, cpr-4</italic>, and <italic>lys-6</italic> were down regulated. Only <italic>dod-22</italic> had a documented role in innate immunity, which demonstrates the merit of our approach in the identification of novel genes that are involved in combating <italic>S. maltophilia</italic> infection.</p>