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Deficiency of double mutant recombinants in crosses of phage T4
Authors:K M Fisher and Harris Bernstein
Institution:(1) Radiobiology Laboratory, University of California, 95616 Davis, California;(2) Department of Microbiology College of Medicine, University of Arizona, 85721 Tuseon, Arizona
Abstract:Summary Only 1.4% of the double mutant recombinants expected on the basis of wild-type recombination frequencies were observed in the combined data from two-factor crosses between a gene 37 amber mutant, amB280, and eighteen different temperature sensitive mutants which were also defective in gene 37. Similar, though less extreme, deficiencies of double mutant recombinants were observed by Doermann and Parma (1968) for mutants in several other genes. In our amB280xts crosses, frequencies of wild-type recombinants were in reasonably good agreement with those expected from the map positions of the mutants determined in crosses not involving amB280. Wild-type and double mutant recombinants were found at comparable frequencies when each of three other gene 37 amber mutants was crossed to a gene 37 temperature sensitive mutant.Experiments were performed to test whether the deficiency of double mutant recombinants in the amB280xts crosses could be explained by assuming that they occurred primarily in heterozygous particles, where their expression was masked. However, no evidence in support of this explanation was found. Other possible explanations, that the deficiency of double mutants was due to their inviability or the inability of double mutant chromosomes to replicate, were also inconsistent with our observations. The hypothesis considered to most plausibly explain our evidence is that the process by which double mutant recombinant chromosomes are formed is inhibited in the vicinity of a poorly suppressed am mutation.
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