K A O'Connor

Starvation-independent sporulation in Myxococcus xanthus involves the pathway for beta-lactamase induction and provides a mechanism for competitive cell survival.

Myxococcus xanthus is a Gram‐negative, soil‐dwelling bacterium with a complex life cycle which includes fruiting body formation and sporulation in response to starvation. This developmental process is slow, requiring a minimum of 24–48 h, and requires cells to be at high cell density on a solid surface. It is known that, in the absence of starvation, vegetatively growing cell suspensions can form ‘glycerol spores’ when exposed to high levels of glycerol, usually 0.5 M. The cells differentiate from rods to resistant spheres rapidly (2–4 h) and synchronously. We have found that the chromosomally encoded β‐lactamase of M. xanthus can be induced by numerous β‐lactam antibiotics as well as by non‐specific inducers including glycine and many D‐amino acids. In addition, D‐cycloserine, phosphomycin, and hen egg‐white lysozyme also induce β‐lactamase in this bacterium. Unexpectedly, agents which induce β‐lactamase can induce ‘glycerol spores’; all of the agents tested which induce glycerol spores (glycerol, DMSO, ethylene glycol) also induce β‐lactamase. During the induction of sporulation, β‐lactamase activity increases, reaching a peak during the morphological transition from rod‐shaped cells to spherical spores. These spores are viable and resistant to many treatments which disrupt vegetatively growing rods but are not as resistant as fruiting body spores. The concomitant induction of β‐lactamase and starvation‐independent sporulation suggests that these processes share a common signal‐transduction pathway. These results also suggest that starvation‐independent sporulation may be an adaptation of cells in order to resist agents that damage peptidoglycan structure and therefore threaten cell survival.

Developmental aggregation of Myxococcus xanthus requires frgA, an frz-related gene.

Myxococcus xanthus is a gram-negative bacterium which has a complex life cycle that includes multicellular fruiting body formation. Frizzy mutants are characterized by the formation of tangled filaments instead of hemispherical fruiting bodies on fruiting agar. Mutations in the frz genes have been shown to cause defects in directed motility, which is essential for both vegetative swarming and fruiting body formation. In this paper, we report the discovery of a new gene, called frgA (for frz-related gene), which confers a subset of the frizzy phenotype when mutated. The frgA null mutant showed reduced swarming and the formation of frizzy aggregates on fruiting agar. However, this mutant still displayed directed motility in a spatial chemotaxis assay, whereas the majority of frz mutants fail to show directed movements in this assay. Furthermore, the frizzy phenotype of the frgA mutant could be complemented extracellularly by wild-type cells or strains carrying non-frz mutations. The phenotype of the frgA mutant is similar to that of the abcA mutant and suggests that both of these mutants could be defective in the production or export of extracellular signals required for fruiting body formation rather than in the sensing of such extracellular signals. The frgA gene encodes a large protein of 883 amino acids which lacks homologues in the databases. The frgA gene is part of an operon which includes two additional genes, frgB and frgC. The frgB gene encodes a putative histidine protein kinase, and the frgC gene encodes a putative response regulator. The frgB and frgC null mutants, however, formed wild-type fruiting bodies.