TRANSDUCTION BY BACTERIOPHAGE P1: ABNORMAL PHAGE FUNCTION OF THE TRANSDUCING PARTICLES.

Transduction by bacteriophage, as first described in Salmonella,' is the phagemediated transfer of any one of a number of genetic traits from one bacterial cell to another. The frequency of genetic transfer is quite low, 1: 105-1:108 per infecting phage particle for any one trait. Further study of this phenomenon both in Salmonella and in the coli-dysentery bacteria,2'3. 4, 5 6 showed that closely linked genetic factors can be transduced jointly and that, although transduction can be detected only when the phage particles do not kill the host cell, lysogenization does not necessarily accompany transduction. Other pertinent facts about transduction are summarized in a recent review.7 In the so-called "specialized transduction" of the Gal factors of E. coli by phage X,8, 9a different situation is observed. The Gal genetic region appears to have become intimately associated with the genetic material of the phage, which is thereby made abnormal and defective.10' 11 In the instances of non-specialized transduction, it has never been tested directly whether the transducing particles are normal or not-more specifically, whether they carry and transfer, in addition to the host genetic factors, a normal phage genome. The finding of non-lysogenic transduced cells provides no evidence, because most cells that give a reductive response to a temperate phage12 segregate out phage-carrier and non-carrier cells for many generations.13' 14 Studying transduction by phage P1 in the coli-dysentery group, Lennox5 found evidence of phage abnormalities in transduced bacteria: some tendency to antisegregation, that is, negative correlation between lysogeny and transduced characters in the progeny of transduced cells, as well as the presence of apparently defective lysogens (immune, phage-non-producing cells) among cells of Shigella dysenteriae receiving the Lac+ factor by transduction from Escherichia coli. To investigate the P1 transduction more closely, we studied the segregation of non-phage-carrier cells in the progeny of cells of S. dysenteriae Sh and E. coli K-12 after infection with phages P1 or P1kc, comparing the segregation pattern in clones from unselected cells and from transduced cells. The methods used were similar to those described by Lennox.5 The results were immediately striking. We found that practically all unselected infected cells that do not lyse give pure lysogenic clones. This is true irrespective of the recipient cell, whether Shigella or E. coli K-12; of the multiplicity of infection, from 0.5 to 15; of the genetic markers in the phage, P1 or Plkc; and of the temperature of postinfection incubation, which affects the proportion of lytic versus lysogenic responses.15 The clones of unselected cells were obtained either by random distribution of infected cells into tubes or by selected isolation of single cells by micromanipulation (kindly carried out for us by Dr. D. K. Fraser). The results are shown in Table 1. The only two significantly mixed clones (with comparable numbers of lysogenic and sensitive cells) were found in an experiment where a few large,