Phage‐exclusion enzymes: a bonanza of biochemical and cell biology reagents?

Abstract

Many parasitic DNA elements including prophages and plasmids synthesize proteins that kill the cell after infection by other phages, thereby blocking the multiplication of the infecting phages and their spread to other nearby cells. The only known function of these proteins is to exclude the infecting phage, and therefore to protect their hosts, and thereby the DNA elements themselves, against phage contagion. Many of these exclusions have been studied extensively and some have long been used in molecular genetics, but their molecular basis was unknown. The most famous of the phage exclusions are those caused by the Rex proteins of lambda prophage. The Rex exclusions are still not completely understood, but recent evidence has begun to lead to more specific models for their action. One of the Rex proteins, RexA, may be activated by a DNA-protein complex, perhaps a recombination or replication intermediate, produced after phage infection. In the activated state, RexA may activate RexB, which has been proposed to be a membrane ion channel that allows the passage of monovalent cations, destroying the cellular membrane potential, and killing the cell. We now understand two other phage exclusions at the molecular level which use strategies that are remarkably similar to each other. The parasitic DNA elements responsible for the exclusions both constitutively synthesize enzymes that are inactive as synthesized by the DNA element but are activated after phage infection by a short peptide determinant encoded by the infecting phage. In the activated state, the enzymes cleave evolutionarily conserved components of the translation apparatus, in one case EF-Tu, and in the other case tRNALys.(ABSTRACT TRUNCATED AT 250 WORDS)

Altruism can evolve when relatedness is low: evidence from bacteria committing suicide upon phage infection

“…In combination with the sensor RexA, which is triggered by several unrelated phages [38], the system may have subsequently been coopted into an adaptive suicidal host-defence mechanism. Co-option, which is a common phenomenon in evolution [32], might have also been involved in shaping some of the other Abi systems described in bacteria [9][10][11]. Moreover, it might be that not all Abi systems involve active suicide (i.e.…”

“…From an evolutionary perspective, the expression of an Abi system could reflect an altruistic act that allows infected bacteria to commit suicide in order to prevent parasite transmission to nearby relatives. Bacteria possess a number of Abi mechanisms, which usually involve joint actions by a prophage (a phage integrated into the bacterial genome) or a plasmid that encodes the genes for the abortive infection, and the bacterium, which transcribes and synthesizes the abortive machinery [7][8][9][10][11]. Important to note is that in many cases the interests of the bacterium and an already resident prophage become completely aligned upon obligately lytic phage infection (i.e.…”

Diverse Functions of Restriction-Modification Systems in Addition to Cellular Defense

“…Upon phage infection, a replication complex intermediate activates RexA. Two activated molecules of RexA in turn activate RexB, an ion channel protein (43). The activated RexB reduces the membrane potential of the cell, resulting in the death of the host and the phage.…”

“…The Rex system of E. coli, which contains two components, viz., RexA and RexB, is one of the most well-studied abortive infection systems to date (43,44). Upon phage infection, a replication complex intermediate activates RexA.…”

“…The activated RexB reduces the membrane potential of the cell, resulting in the death of the host and the phage. Other Abi systems of E. coli include the Lit protein and the polypeptide encoded by prr (43).…”