No abstract

R1822, a plasmid specifying multiple drug resistances, has been transferred to a variety of species representative of related and unrelated genera. The host range of the plasmid includes Enterobacteriaceae, soil saprophytes, Neisseria perflava, and photosynthetic bacteria. With the acquisition of drug resistance(s), these strains became sensitive to a small, ribonuclease-sensitive bacteriophage, designated PRR1, isolated by enrichment from sewage. ' Received as PAT 2; spontaneous streptomycin-resistant mutant (1 mg/ml). d Received as PA0602; PAL(R1822) x PA0602. e Auxotrophic mutant of P71 isolated from milk by J. J. Jezeski, Univ. of Minnesota. ' Department of Microbiology, Univ. of Michigan. ' Spontaneous streptomycin-resistant mutant (1 mg/ml). hDepartment of Biochemistry, Univ. of Michigan. colonies from the primary isolation medium (always containing carbenicillin) to TGE agar medium containing tetracycline or neomycin at 50 ug/ml. Mating. R+ strains used in subsequent quantitative estimates of transfer frequencies were constructed by mixed inoculation of TGE broth medium I 773

Four cistrons (adh) involved in the expression of the K88 adhesion system have been identified and mapped. Three of these (adh A, adh B and adh C) are located in a single operon (I) whereas the fourth (adh D) is expressed from a separate promoter (operon II). The polypeptides encoded by these cistrons have been identified and their role in the formation and regulation of K88 fimbriae (pili) is discussed.

Incompatibility group P plasmids demonstrate strong entry exclusion properties. Stringent incompatibility is also observed in the absence of entry exclusion. These observations have been facilitated by the study of a nontransmissible plasmid, RP1-S2, derived from RP1 by transductional shortening. RP1-S2 retains carbenicillin and tetracycline resistances as well as loci that cause either the loss of P plasmids (incp) or a locus specifying susceptibility to curing (sinp) in the presence of a P plasmid. RP1-S2 can be mobilized by an incompatibility group W plasmid, R388, and also freely forms recombinants with R388. P, N, and W incompatibility group plasmids all encode information for the receptor of the cell wall-adsorbing phage PRD1. Based on the premise that the location of this receptor is analogous to entry exclusion factors for F-like plasmids and hence a regulated transfer region determinant, we tested fertility inhibition relationships among these plasmid groups. We detected both reciprocal and nonreciprocal fertility inhibition relationships for bacteria containing various combinations of W, N, and P group plasmids. The nonreciprocal nature of some combinations, we believe, reflects the identity of the point mutation reading to derepression of the plasmid in question. Reciprocal fertility inhibition, on the other hand, may reflect the reconstruction of a fertility inhibition system through complementation. An X incompatibility group plasmid, known to affect the fertility of an N group plasmid, was also shown to inhibit P plasmid fertility. These observations may indicate a possible evolutionary relationship(s) of plasmids unrelated by the criteria of incompatibility, pilus phage specificity, or plasmid host range.

K88 antigen, an important virulence factor in porcine enteropathogenic Escherichia coli (EEC), can be transferred along with the ability to ferment the trisaccharide raffinose (Raf). The plasmids from a number of EEC strains that encode these two properties were isolated and characterized. In most strains the K88 and Raf genes were found on a single nonconjugative plasmid approximately 50 x 106 daltons in size. This plasmid core was conserved with only slight variation among the strains tested. In some transconjugants, larger conjugative plasmids were observed that were apparently recombinants between the Raf/K88 plasmid and a transfer factor. Occasionally plasmids carrying only the raffinose fermentation genes arose by deletion of a deoxyribonucleic acid segment of about 20 x 106 daltons that included the K88 antigen gene(s).on August 1, 2020 by guest http://iai.asm.org/ Downloaded from