Serratia marcescens HY bacteria must be lysogenic with either prophage y or psi to make it possible for phage kappa to form plaques unless they carry a so-called ink mutation. Genes in y and psi termed any and anp were identified that after infection of ink+ cells are necessary for an effective propagation of these phages as well as of coinfecting kappa phage. When kappa infects y and/or psi-lysogenic cells it transactivates the respective prophage genes by means of two early genes termed tay and tap. It appears that on infection of nonlysogenic ink+ cells kappa damps its own development, provided the regulatory region of the responsible gene is undermethylated. After kappa infection duly to achieve the special methylation of this region seems to be the function of any and anp. There are some more genes in y and psi prophage under the control of tay and tap, concerning in both cases a Dam methylation (recognition sequence GATC) of kappa DNA, a recombination proneness under restricting conditions of kappa DNA not modified by the modification enzyme of HY, and the kappa plaque size. By hybridization studies a region of homology common to y and psi was demonstrated which from its size might comprise all the transactivated genes. The view is supported by genetic data indicating an affinity among the any and anp genes. Investigation of various any mutants were indicative of DNA inversions in this region of the y genome. Surprisingly some of the any mutants had become sensitive in their plaque forming ability to an inhibitory activity exerted by prophage psi. Mutants of psi unable to interfere but still able to lysogenize were isolated. A model is presented accounting for the formation of pleiotropic and nonpleiotropic mutations with Any phenotype and their reversion types. Possible functions of the y genes and their counterparts in psi are discussed.
Plaque formation of phage x on Serratia marcescens strain H Y normally depends on the presence of either a y or y prophage in the indicator bacteria. Bacterial ink mutants allowing x growth in the absence of either prophage were isolated from the doubly cured strain H Y (y, y)-. By means of a x mutant, named qdy, a n active participation of x in antagonizing inhibition of its own growth on HY (y, y)was demonstrated. The qdy mutation is closely linked to gene CIII coding for the x repressor. The prophages y and y enable x t o grow undisturbed probably by modifying the x DNA 1) Abbreviations: moi = multiplicity of infection; eop = efficiency of plating; NB = nutrient broth
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