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Originally published as Genetics Published Articles Ahead of Print on December 6, 2006.
Genetics, Vol. 175, 681-697, February 2007, Copyright © 2007
doi:10.1534/genetics.106.060087
Mos1 Mutagenesis Reveals a Diversity of Mechanisms Affecting Response of Caenorhabditis elegans to the Bacterial Pathogen Microbacterium nematophilum
Karen Yook and Jonathan Hodgkin1
Genetics Unit, Department of Biochemistry, University of Oxford, Oxford OX1 3QU, United Kingdom
1 Corresponding author: Genetics Unit, Department of Biochemistry, University of Oxford, S. Parks Rd., Oxford OX1 3QU, United Kingdom.
E-mail: jonathan.hodgkin{at}bioch.ox.ac.uk
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 bacterially unswollen (Bus) 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.
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Genetics 2007 175: NP.
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