Isolation and characterization of a generalized transducing phage for Xanthomonas campestris pv. campestris.

We have isolated and characterized a lytic double-stranded DNA Xanthomonas campestris pv. campestris bacteriophage (XTP1) capable of mediating generalized transduction. The phage transduces chromosomal markers at frequencies of 10(-5) to 10(-6) transductants per PFU.

Rhizobium meliloti exoG and exoJ mutations affect the exoX-exoY system for modulation of exopolysaccharide production.

R. meliloti Rm1021 normally produces an acidic Calcofluor-binding exopolysaccharide, called succinoglycan or EPS I, which is required for successful nodulation of alfalfa by this strain. At least 13 loci affecting production of EPS I were previously mapped to a cluster on the second of two symbiotic megaplasmids in Rm1021, pRmeSU47b.

A repetitive DNA sequence, rhs, responsible for duplications within the Escherichia coli K-12 chromosome.

A novel family of large, imperfectly repeated DNA sequences has been found in Escherichia coli. Two members of this family, rhsA and rhsB, occur as direct repeats, flanking the pit glyS xyl segment of the chromosome. Unequal sister-chromatid crossing over between rhsA and rhsB accounts for the frequent tandem duplication of the glyS locus that has been observed by various workers.

SOS induction by P1 Km miniplasmids.

We have constructed (in vitro) a set of P1 miniplasmids. The smallest of these that could function as an independent replicon contained the right side of EcoRI-5 plus all of EcoRI-8. Those miniplasmids that lack EcoRI-6 induce the SOS pathway of the cell as shown by (i) increased expression of the recA operon, (ii) excision of the cryptic genetic element e14, (iii) spontaneous induction of lambda, and (iv) dependence of e14 excision on recA+ function.

F sex factor of Escherichia coli K-12 codes for a single-stranded DNA binding protein.

In Escherichia coli K-12 strains that carry the mutation ssb-1 in the gene for single-stranded DNA binding protein, the presence of the F sex factor partially reverses the temperature-sensitive growth phenotype caused by the mutation. The region of F (EcoRI fragment 3) responsible for this compensation has been identified and subcloned onto pBR322. A BamHI cleavage site has been found to intersect the essential coding region for this F function.