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doi:10.1534/genetics.106.060087
A more recent version of this article appeared on February 1, 2007.
REGULAR RESEARCH PAPERS |
Mos1 mutagenesis reveals a diversity of mechanisms affecting response of C. elegans to the bacterial pathogen M. nematophilum
Karen Yook 1 and Jonathan Hodgkin 1*
1 University of Oxford
* To whom correspondence should be addressed. E-mail: jah{at}bioch.ox.ac.uk.
Submitted on April 27, 2006
Revised on June 23, 2006
Accepted on 15 November 2006
A specific host-pathogen interaction exists between Caenorhabditis elegans and the Gram-positive bacterium Microbacterium nematophilum. This bacterium is able to colonize the rectum of susceptible worms and induces a defensive tail-swelling response in the host. Previous mutant screens have identified multiple loci that affect this interaction. Some of these loci correspond to known genes, but many bus genes (those with a Bus (Bacterially Un-Swollen) mutant phenotype) have yet to be cloned. We employed Mos1 transposon mutagenesis as a means of more rapidly cloning bus genes and identifying new mutants with altered pathogen response. This approach revealed new infection-related roles for two well-characterized and much studied genes, egl-8 and tax-4. It also allowed the cloning of a known bus gene, bus-17, which encodes a predicted galactosyltransferase, and of a new bus gene, bus-19, which encodes a novel, albeit ancient, protein. The results illustrate advantages and disadvantages of Mos1 transposon mutagenesis in this system.
Key Words: C. elegans, Infection, Innate immunity, Mos1 mutagenesis, Surface coat
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