This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. The subproject and investigator (PI) may have received primary funding from another NIH source, and thus could be represented in other CRISP entries. The institution listed is for the Center, which is not necessarily the institution for the investigator. The C. elegans cuticle is infected by the nematode bacterial pathogen Microbacterium nematophilum. In screens for C. elegans mutants with altered susceptibility to infection several bus (bacteria unswollen) mutants were isolated with increased resistance to infection. DNA sequencing experiments and homology searches suggest strongly that glycoconjugate biosynthetic enzymes may be disrupted in these mutants. The srf-3 mutants contain genetic lesions in a Golgi nucleotide sugar transporter and are also resistant to M. nematophilum infection, supporting the notion that the bus phenotype is due to a loss of function in one or more glycoconjugate pathways. We have begun analysis of the glycoconjugates of the several bus mutants. As homology does not necessarily accurately predict function we plan to investigate several glycoconjugate classes in tandem. Analyses will include mass spectrometric analysis of N- and O-glycans and glycosphingolipids of the mutants compared to those of the wild-type C. elegans N2 bristol strain using methods w have developed and adapted to the C. elegans model.
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