Genetic suppression and phenotypic masking of a Myxococcus xanthus frzF‐ defect

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Abstract
Summary: An insertion of transposon Tn5‐lac, ω4519, generates a lacZ fusion with a Myxococcus xanthus promoter expressed during both vegetative growth and development. Sequence analysis of the junction of ω4519 with M. xanthus DNA shows that the insertion is in frzF, a homologue of cheR from Salmonella typhimurium. When frzF‐ (or frzCD‐) cells are starved for nutrients at modest densities, they aggregate to form a radial pattern and produce fewer than 1% of the wild‐type complement of spores. At higher densities, frzF::ω519 cells form‘frizzy’aggregates and produce 80–90% of the wild‐type complement of spores. In contrast, when cells with both a frzF‐ (or frzCD‐) and an sgtA1 mutation are allowed to develop at either low or high cell densities, they produce frizzy aggregates containing a near wild‐type complement of heat‐resistant spores. In addition to suppressing the density dependence of fruiting‐body morphogenesis, the sglA1 mutation also suppresses the sporulation defect caused by two different frzF‐ mutations and a frzCD‐ mutation. In contrast, a mutation in a different S motility gene, sglG1, does not suppress the frz‐ mutations. Thus, the suppression of frz‐ mutations by sgl‐ mutations is allele‐specific, and depends on the sgl allele, but not the frz allele. Because the phenotypes of frz‐ mutations have been determined in a (suppressing) sglA1 genetic background, the frz genes may play more central roles in development than initially recognized.