Chapter 23 Notes: Evolution of Genetic Systems: Figure WN23.4 - Possible mutational mechanism responsible for LPS phase variation in H. influenzae, based on slipped-strand mispairing (Levinson and Gutman 1987; Weiser et al. 1989).

Figure WN23.4 - Possible mutational mechanism responsible for LPS phase variation in H. influenzae, based on slipped-strand mispairing (Levinson and Gutman 1987; Weiser et al. 1989).

Figure WN23.4. Possible mutational mechanism responsible for LPS phase variation in H. influenzae, based on slipped-strand mispairing (Levinson and Gutman 1987; Weiser et al. 1989). The DNA sequence of the 5′ end of the H. influenzae lic2 gene, required for the biosynthesis of a Galα(1-4)Galβ disaccharide in the LPS core (High et al. 1993), is shown. Phase variation of the digalactoside is mediated through changes in the number of copies of tandem repeats of CAAT (bold); 16 copies of the tetranucleotide sequence are shown. Potential translational start codons (boxed ATG) for a long open reading frame are shown and are positioned such that ATG 1 and 2 are in-frame when lic2 has 16 copies of CAAT, ATG 3 is in frame if lic2 has 17 copies of CAAT, and there is no ATG in-frame if there are 15 copies of CAAT. (Reproduced from Fig. 3 of Moxon et al. 1994.)

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