Worm Breeder's Gazette 17(3): 38 (November 1, 2003)

These abstracts should not be cited in bibliographies. Material contained herein should be treated as personal communication and should be cited as such only with the consent of the author.

Plague? Bah! Mutants resistant to the bubonic plague biofilm

Creg Darby

Department of Microbiology, University of Alabama at Birmingham, BBRB 632, 1530 3rd Avenue S., Birmingham, AL 35226-2170. creg@uab.edu

Bubonic plague is spread by the bites of fleas infected with Yersinia pestis bacteria. When worms are exposed to Y. pestis, sticky biofilms appear on their heads. The biofilms cover mouths and impair feeding, which in the case of larvae delays or arrests growth. Bacterial genes required for flea infection are also required to form worm biofilms, suggesting that the plague-flea interaction can be modeled with C. elegans (1).


N2 worms were mutagenized with ENU and the F2 eggs were deposited on lawns of Y. pseudotuberculosis, a close relative of the plague bacillus that also produces biofilms. We screened for animals that had no biofilm and grew normally in the continuous presence of Yersinia, a phenotype we call Bah: Biofilm Absent on Head. We obtained 11 independent Bah mutants from 7,000 mutagenized genomes, a frequency that suggests mutations in multiple genes. There are no obvious secondary phenotypes in the mutants.


Biofilms appear on the exterior of worms, and Yersinia does not colonize interior tissues, suggesting that some Bah mutants will have altered surface characteristics. Furthermore, three mutations affecting the worm surface -- srf-2, srf-3, and srf-5 -- have been shown to confer resistance to adherent infection by the nematode pathogen Microbacterium nematophilum (2). We found that animals with the same three srf mutations are Bah. Because the bacterial genera Microbacterium and Yersinia are not closely related, this commonality suggests that srf-2, srf-3 and srf-5 are important in a variety of interactions between nematodes and bacteria.


1. Darby et al. (2002) Nature 417:243-44.

2. Hodgkin et al. (2001) Current Biology 10:1615-18.