Transposon insertions located 325 and 740 base pairs upstream of the transcriptional start site of the flhDC operon resulted in cells that initiated swarming 1.5h earlier than wild-type and exhibited a 2-2.5-fold greater swarming velocity. These mutants also failed to consolidate (de-differentiate) normally and did not form the characteristic bulls-eye pattern of concentric swarming rings on solid media. The analysis of one mutant (SS-P) with an insertion at -325 revealed that the levels of flhDC mRNA were dramatically higher than wild-type during swarmer cell differentiation and failed to decrease during the consolidation period. However, the start point of flhDC transcription was identical in the SS-P mutant and wild-type cells. The presence of the flhDC upstream region on a high copy plasmid increased swarming motility and expression of a chromosomal flhDC-lacZ fusion, presumably by titrating out a repressor. To identify potential repressors and further define flhDC regulation in P. mirabilis, targeted disruptions were created in the rcsB, ompR, lrhA and hdfR genes, previously demonstrated to repress flhDC in E. coli. Of these mutations, only the loss of rcsB increased swarming and flhDC mRNA accumulation.