Transcriptional control of capsid size in the P2:P4 bacteriophage system

Abstract

Satellite virus P4 is a defective bacteriophage which utilizes all of the 17 known morphogenic genes of a helper phage such as P2 to construct its virion (Six, 1975). In so doing, it causes the products of some of these genes to condense into an icosahedral capsid one-third the size of that produced by the P2 helper itself (Inman et al., 1971; Shore et al., 1978). It has also been shown that P4 wild-type suppresses the very strong polarity normally associated with certain amber mutations in the morphogenic gene operons of P2 (Sunshine et al., 1976). Such polarity is known to be mediated by the Escherichia coli transcription factor rho (Richardson et al., 1975; Korn & Yanofsky, 1976 b; Adhya et al., 1976; Guarente et al., 1975). This paper demonstrates that: (1) P4 sid1, a mutant which cannot cause the production of small capsids (Shore et al., 1978), has also lost most of the P4 wild-type ability to suppress the polarity of P2 late gene amber mutations; (2) the size-directing lesion in P4 sid1 is bypassed by a host rho mutation, since small capsids are produced after P4 sid1 infection of a P2 lysogen carrying this rho mutation; and (3) the lack of normal termination of transcription exhibited by this same rho mutation is sufficient to force the production of small P4-sized capsids, since they are produced after infection of this host by P2 alone. The results suggest that the choice between two distinct capsid sizes produced from the same gene products is mediated by an effect at the level of transcription termination which in turn regulates the relative levels of gene products. P4 apparently influences this choice by producing an antitermination factor whose function is rendered defective by the P4 sid1 mutation. Our results in this area are interesting because they present a clear example of the biological consequences resulting from such modulations in transcription termination. The consequences in this case, i.e. virion capsid size determination, suggest that transcriptional control at this level may be an unexpected but important mechanism involved in regulation of the assembly and function of complex biological structures.