To test the hypothesis that actA allelic variation contributes to virulence differences among Listeria monocytogenes strains, cell-to-cell spread and intracellular ActA phosphorylation patterns were characterized for 14 wild-type isolates and selected isogenic mutants. Our data show that (i) while actA allelic variation is not responsible for enhanced cell-to-cell spread observed in epidemic clone I strains, actA allelic variation may contribute to reduced plaque size observed in some isolates, (ii) actA sequence alone determines phosphorylation-dependent ActA banding patterns, and (iii) sequence variation at the positively selected ActA residue 498 does not contribute to ActA phosphorylation patterns or to differences in cell-to-cell spread.
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Roberts et al. (2006) studied this question.