We have shown that the plasmid pSC101 is unable to be maintained in strains of E. coli carrying deletions in the genes himA and hip which specify the pleitropic heterodimeric DNA binding protein, IHF. We show that this effect is not due to a modulation of the expression of the pSC101 RepA protein, required for replication of the plasmid. Inspection of the DNA sequence of the essential replication region of pSC101 reveals the presence of a site, located between the DnaA binding-site and that of RepA, which shows extensive homology with the consensus IHF binding site. The proximity of the sites suggests that these three proteins, IHF, DnaA, and RepA may interact in generating a specific DNA structure required for initiation of pSC101 replication.

In pneumococcal transformation, recombination frequency between point mutations is usually proportional to physical distances. We have identified an aberrant marker belonging to the amiA locus that appeared to markedly enhance recombination frequency when crossed with any other markers of this gene. This mutation results from the C-to-A transversion in the sequence A-T-T-C-A-T -+ A-T-T-A-A-T. This effect is especially apparent for short distances as small as 27 base pairs. The hyperrecombination does not require the wild-type function of the pneumococcal gene for an ATP-dependent DNase (which is homologous to the product of the Escherichia coli recBC genes) or of the hex genes, which correct certain mismatched bases in transformation. The hyperrecombination is affected by the presence of nearby mismatched bases that trigger an excision-repair system. It is proposed that the mutation that shows hyperrecombination is sometimes converted to the wild-type allele at the heteroduplex stage of transformation.General recombination involves the exchange of genetic information between homologous DNA segments. The frequency of recombination has been postulated to be approximately constant throughout homologous regions. However, this assumption is not always true, as has been shown by genetic studies. Many examples of map distortions have been reported. In fungi as well as other eukaryotes, the frequency of exchange between genes can be strongly affected by mutations (1). The nature of the genetic factors controlling the recombination events has remained elusive. A major step in the molecular understanding of one such factor has been the studies by Stahl and his collaborators of sites (Chi elements) that promote recombination in bacteriophage X (2). Such sites are also found in the Escherichia coli chromosome and may affect bacterial recombination (3). It was found that the enhancement of recombination due to Chi sites was asymmetric, and it required the wild-type activity of recBC genes. A specific octamer is present in all reported Chi elements (3). Recombination hotspots also have been observed in recombination between E. coli plasmids. These hotspots appear to be different from Chi elements in that they do not require the recBC pathway and they are active in either orientation (4). Moreover, Lieb identified mutations that enhance recombinations in bacteriophage crosses (5). Such mutations are particularly susceptible to mismatch correction by short patch repair and are quite different from the Chi elements. In studies of marker effects in bacteriophage T4 recombination, short patch repair has also been reported (6,7). Therefore, it appears that there are a variety of factors that control recombination, which may be more or less specific to the organism under investigation. Moreover, the mechanisms of enhanced recombination could be better understood if genes that promote such an effect were known.The subject of this report is the description of a mutation belonging to the amiA locus of Streptococcus pneumoniae t...

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