GENETIC SUPPRESSION AND PHENOTYPIC MASKING OF A MYXOCOCCUS-XANTHUS FRZF(-) DEFECT

An insertion of transposon Tn5-lac, Omega 4519, generates a lacZ fusion with a Myxococcus xanthus promoter expressed during both vegetative growth and development, Sequence analysis of the junction of Omega 4519 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 wildtype complement of spores. At higher densities, frzF::Omega 4519 cells form 'frizzy' aggregates and produce 80-90% of the wild-type complement of spores, In contrast, when cells with both a frzF(-) (or fizCD(-)) and an sglA1 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.