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Herman Lab

Research in the Herman Lab

We use the nematode Caenorhabditis elegans as a model to study animal development, behavior and species interactions. We're interested in the genetic, evolutionary and ecological basis for organismal interactions within a community of soil organisms. We've focused on the interactions of bacterivorous nematodes, important members of the soil decomposition food web, with soil bacteria, which serve not only as food sources but also as potential pathogens. We use both field-based and laboratory approaches to understand the gene functions involved in the formation and maintenance of dynamic soil nematode communities in changing environments.

Recently we have focused our efforts on the study of the interaction between bacterivorous nematode Caenorhabditis elegans and the ubiquitous and emerging nosocomial bacterial pathogen Stenotrophomonas maltophilia. We aim to elucidate the genes that C. elegans employs to respond to pathogenic bacteria in the environment and are using the interaction with S. maltophilia as a model. The study of this interaction has ecological and medical relevance as S. maltophilia and other members of the Stenotrophomonas genus are found in association with C. elegans and other Rhabditids in the wild (Dirksen et al., 2016; Samuel at al., 2016) and S. maltophilia has been isolated from various clinical sources. We found a local S. maltophilia isolate (JCMS) in association with grassland soil nematodes to be more virulent than the other S. maltophilia isolates we tested. The C. elegans response to the virulent S. maltophilia strain JCMS requires the action of several conserved innate immune pathways that serve to protect the nematode from other pathogenic bacteria. However, insulin-like DAF-2/16 signaling pathway mutants that are typically pathogen resistant are susceptible to JCMS, and several DAF-2/16 regulated genes are not significantly differentially expressed in response to JCMS (White et. al. 2016). This indicates that JCMS evades the pathogen resistance conferred by loss of DAF-2/16 pathway components (White et al., 2016). 

To better understand the C. elegans-S. maltophilia interaction and identify the specific genes C. elegans employs in its response to S. maltophilia, we identified genes differentially expressed under different bacterial treatments to find genes that might explain how JCMS evades the DAF-2/16 pathway. We are using a probabilistic functional gene network model (Lee et al., 2008, 2010) to help determine which differentially expressed genes might be central to the C. elegans response to S. maltophilia and are testing those genes for function in the interaction.