Lysogenic Cycle

9 Key excerpts on "Lysogenic Cycle"

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  eBook - ePub

  Thinking Like a Phage

  The Genius of the Viruses That Infect Bacteria and Archaea

  • Merry Youle, Leah L Pantéa(Authors)
  • 2017(Publication Date)
  • Wholon

    (Publisher)

  Chapter 8.

  Coalition

  In which

  the phage foregoes immediate, prolific replication and instead settles in as a prophage embedded within the virocell chromosome. The prophage replicates, but slowly. One prophage becomes two, two become four, and so on, in step with virocell division. While on board, a prophage silences those of its genes that drive its lytic infection cycle, and expresses those that benefit the virocell of which it is a part. If conditions deteriorate and virocell survival is endangered, it terminates its lease, resumes its own rampant replication, and lyses the virocell to free its progeny.

   

  Lysogeny is the hereditary power to produce bacteriophage. A lysogenic bacterium is a bacterium possessing and transmitting the power to produce bacteriophage…Prophage is the form in which lysogenic bacteria perpetuate the power to produce phage.

  André Lwoff 1953 Thus, prophages are not solely dangerous molecular time bombs that can bring about cell mortality, but also serve as a key to bacterial survival in the oligotrophic oceans. John Paul 2008 Politeness is the poison of collaboration. Edwin Land Any coalition, especially where one party is more powerful than the other, it’s always bound to have a pecking order. Peter Hook

   

  A re takeover and immediate replication always the best infection tactics for a phage? Rapid production and release of abundant progeny virions is one way to counter the low probability of a successful quest, but might there be a better way to utilize host resources, at least under some conditions? Many phages, possibly the majority, say “yes.” These are the temperate phages. Each time a temperate phage arrives in a host cell, it chooses between the two alternative pathways available to it: lysis and lysogeny. Like the strictly lytic phages, it can immediately launch a lytic infection complete with the usual chromosome replication, production of phage proteins, assembly, and ultimate virocell destruction by lysis. On the other hand, it can opt for the lysogenic alternative – a substitute for the single-minded pursuit of maximum short-term gain. Here the phage resides quietly inside the virocell for an indefinite period of time while the newly formed phage-host coalition perks along. The virocell, now called a lysogen,1

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  Snyder and Champness Molecular Genetics of Bacteria

  • Tina M. Henkin, Joseph E. Peters(Authors)
  • 2020(Publication Date)
  • ASM Press

    (Publisher)

  Gottesman , Suggested Reading).

  Figure 7.21 gives an overview of the two life cycles of which λ is capable and the fate of the DNA in each cycle, while Figure 7.22 gives a more detailed map of the phage genome for reference. As described above, phage λ DNA is linear in the phage head, and the map shows how it exists in the head. Immediately after the DNA is injected into the cell to initiate the infection, the DNA cyclizes, that is, forms a circular molecule, by pairing between the cos sites at the ends (Figure 7.9 ). This brings the lysis genes (S and R) and the head and tail genes (A to J) of the phage together and allows them all to be transcribed from the late promoter pR ′, as discussed above. This circular DNA can then either integrate into the host chromosome (Lysogenic Cycle) or replicate and be packaged into phage heads to form more phage (lytic cycle). Which decision is made depends on the physiological state of the cell, as we discuss below. Later, the integrated DNA in a lysogen can also be excised, replicate, and form more phage (induction).

  THE LYSIS-LYSOGENY DECISION

  Figure 7.23 illustrates the process of forming a lysogen after λ infection, how the cI, cII, and cIII gene products are involved, and the central role of the CII protein. After λ infects a cell, the decision about whether the phage enters the lytic cycle and makes more phage or forms a lysogen depends on the outcome of a competition between the product of the cII gene, which acts to form lysogens, and the products of the cro gene and of genes in the lytic cycle that replicate the DNA and make more phage particles. Which pathway wins most often depends on the conditions of infection. At a low multiplicity of infection (MOI; see “Multiplicity of Infection” below), the lytic cycle usually wins, and in as many as 99% of the infected cells, the λ DNA replicates and more phage are produced. However, for reasons we explain below, at a high MOI, the CII protein wins more often, and as many as 50% of the infected cells can form lysogens. The richness of the medium also plays a role. One reason is that cells that are growing very fast in rich medium have more RNase III (see chapter 2 ) than if they are growing more slowly, and more RNase III means more N protein, which favors lytic development (see “λ N-Mediated Antitermination” above; Court et al ., Suggested Reading). The reason they have more N protein is that the leftward transcript from pL contains the nutL site just upstream of the translational initiation region (TIR) for the N gene (Figure 7.10 ). The Nus factors and N protein bound to the nutL site inhibit N translation from the nearby TIR for the N gene, so less N protein is made. There is a cleavage site for RNase III between the nutL site and the TIR for gene N, and the higher concentrations of RNase III when the cells are growing rapidly cleave the mRNA at a hairpin between the nutL site and the TIR for gene N, separating the nutL site from the N

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  Genetic Mechanisms of Development

  • Frank H. Ruddle(Author)
  • 2013(Publication Date)
  • Academic Press

    (Publisher)

  1. Brief outline of phage development. After a common early stage, the lytic and lysogenic pathways diverge, either to create more phage particles or to produce the repressed, integrated prophage. The developmental process may be started anew either by another phage infection or by derepression of the prophage. -PROPHAGE I I I I I REGULATION OF BACTERIOPHAGE λ DEVELOPMENT 3 synthesis is followed by a repression of the viral genes and an integration of the viral DNA into the host DNA through a site-specific recombination event. Once established, this prophage state is quite stable under normal growth conditions. However, reversal can occur through a derepression of the viral genome, excision of the phage DNA from the host DNA, and lytic develop-ment as for an infected nonlysogenic cell. Thus the lysogenic path-way has three stages. The period after infection until the establish-ment of the prophage state is termed the establishment of lysogeny, the stable prophage state and its subsequent inheritance is termed the maintenance of lysogeny, and the reversal of this process is termed induction. The temporal organization of the lytic pathway noted above also serves the multiple needs of the lysogenic pathway, for it allows an efficient consummation of each stage of the lysogenic pathway under the appropriate conditions. This aspect will be considered in Section IV. III. THE LYTIC PATHWAY The regulatory problem of the lytic pathway is the temporal organization into a replication-oriented early phase and an en-capsulation-oriented late phase. Our current picture of the major regulatory events during the lytic pathway is presented in Fig. 2. The horizontal line denotes a DNA molecule. The genes are shown in the main generically along the line—clusters of genes involved in head structure, tail structure, genetic recombination, regulatory events, DNA synthesis, and lysis. During the lytic path-way there are three definable stages.

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  Bacteriophages

  Biology and Applications

  • Elizabeth Kutter, Alexander Sulakvelidze, Elizabeth Kutter, Alexander Sulakvelidze(Authors)
  • 2004(Publication Date)
  • CRC Press

    (Publisher)

  holin—a protein that assembles pores in the inner membrane at the appropriate time to allow the lysin to reach the peptidoglycan layer and precipitate lysis. The timing is affected by growth conditions and genetics; mutants with altered lysis times can be selected. The general mechanisms and wide variety of holins and lysins are discussed in detail in Chapter 7. The tailless phages encode a variety of single-protein lysis-precipitating proteins that subvert host peptidoglycan-processing enzymes in various ways.

  3.4. LYSOGENY AND ITS CONSEQUENCES

  The concept of lysogeny has had a checkered history. Early phage investigators in the 1920s and 1930s claimed to find phages irregularly associated with their bacterial stocks and believed that bacteria were able to spontaneously generate phage, which were thus long considered by many to be some sort of “ferment” or enzyme rather than a living virus. When Max Delbrück and his companions began their work, they confined themselves to the classical set of coliphages designated T1–T7, none of which showed this property, and Delbrück attributed the earlier reports to methodological sloppiness. However, the phenomenon could no longer be denied after the careful work of Lwoff and Gutmann (1950); through microscopic observation of individual cells of Bacillus megatherium in microdrops, they demonstrated that cells could continue to divide in phage-free medium with no sign of phage production, but that an occasional cell would lyse spontaneously and liberate phage. Lwoff named the hypothetical intracellular state of the phage genome a prophage and showed later that by treating lysogenic cells with agents such as ultraviolet light, the prophage could be uniformly induced to come out of its quiescent state and initiate lytic growth. The prophage carried by a bacterial strain is given in parentheses; thus, K(P1) means bacterial strain K carrying prophage P1.

  Esther Lederberg (1951) showed that strains of E. coli K-12 carried such a phage, which she named lambda ( λ ). Meanwhile, Jacob and Wollman (1961) had been investigating the phenomenon of conjugation between donor (Hfr) and recipient (F- ) strains of E. coli. They found that matings of F- strains carrying λ and non-lysogenic Hfrs proceeded normally, but that reciprocal matings yielded no recombinants and, in fact, produced a burst of lambda phage. A mating of Hfr( λ ) by non-lysogenic F- would proceed normally if it were stopped before transfer of the gal (galactose metabolism) genes, but if conjugation proceeded long enough for the gal genes to enter the recipient cell, the prophage would be induced (zygotic induction). These experiments indicated that the λ prophage occupies a specific location near the gal genes; that a lysogenic cell maintains the prophage state by expression of one λ gene, encoding a specific repressor protein, which represses expression of all other λ genes; and that if the gal genes—and thus the λ prophage—are transferred into a non-lysogenic cell during mating, the prophage finds itself in a cytoplasm lacking repressor and therefore expresses its other genes and enters the lytic cycle. Typical plaques made by phage λ are turbid, due to lysogenization of some bacteria within the plaque. Mutants of λ producing clear plaques are unable to lysogenize. Analysis of these mutants revealed three genes, designated cI, cII, and cIII, whose products are required for lysogeny. The cI gene encodes the repressor protein. Allen Campbell demonstrated that the sequence of genes in the prophage is a circular permutation of their sequence in the phage genome. He therefore postulated that the prophage is physically inserted into the host genome by circularization of the infecting genome followed by crossing-over between this genome and the (circular) bacterial genome. We now know that the genome in a λ virion has short, complementary single-stranded ends; as one step in lysogenization, it circularizes through internal binding of these ends and is then integrated (by means of a specific integrase) at a point between the gal and bio

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  Advances in Biological and Medical Physics

  Volume 7

  • Cornelius A. Tobias, John H. Lawrence, Cornelius A. Tobias, John H. Lawrence(Authors)
  • 2013(Publication Date)
  • Academic Press

    (Publisher)

  Rather, one may infer that very little, if any, of the phage DNA introduced into the sensitive cell finds incorporation into the prophage to which it gives rise. In fact, the similarity of the stabiliza-tion to inactivation by P^^ decay of lytic and lysogenic centers during the early stages of intracellular phage development suggests that also in the lysogenic response the infecting phage first enters the vegetative state. Hence if the genetic structures of the prophage contain an amount of D N A equal to that of the extracellular phage (a question which will be examined below), then the D N A of the prophage established in a lysogenic response is not the DNA of the infecting virus but one of its vegetative repHcas. Numerous physiological and genetic observations support this conclusion (Lieb, 1953; Bertani and Nice, 1954; Jacob et α/., 1957; Zinder, 1958). DECAY IN BACTERIAL VIRUSES AND BACTERIA 63 DAYS 10 15 20 25 LYSOGENICS • ' • ' i _ l U 0 02 0.4 0.6 0 0.2 0.4 0.6 I'é ^U FRACTION OF P^^ATOMS DECAYED ) FIG. 21. Survival at — 196°C. as lytic and lysogenic centers of E. coli K12S bacteria infected with P^^-labeled λ bacteriophage (parent) (Ao = 600 mC./mg.) and incu-bated for various periods of time (minutes) at 37°C. before freezing (Stent and Fuerst, 1956). C, Immunity The presence of the prophage confers on the lysogenic cell not only the ability to produce infective phage at some later time, but it also renders the bacterium immune toward infection by exogenous phage particles closely related to the carried prophage. Although phage particles adsorb and inject their DNA into the immune lysogenic cell, the viral genome does not appear to multiply (Jacob and Wollman, 1953; Bertani, 1954). If the prophage is induced, however, then immunity is abolished and both endog-enous and exogenous phage multiply and produce infective progeny.

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  Bacillus Subtilis

  • David Dubnau(Author)
  • 2012(Publication Date)
  • Academic Press

    (Publisher)

  These phage particles can transfer the bac-terial genes to new bacteria. This process is called specialized trans-duction, and the particles that carry it out are called specialized trans-ducing particles (TPs). The process is of interest and importance for two reasons. First, the transductants produced in specialized transduction and their progeny are frequently diploid for the bacterial genes carried by the phage. This permits the production of heterogenotes, which allow the experimenter to study the dominance-recessiveness relations of different alleles within a gene and to determine whether closely linked mutations lie within a single cistron. Second, during the lytic part of the phage life cycle the bacterial genes carried by a transducing phage replicate under phage control. This permits amplification of the bacterial genes. Specialized transduction was first observed with phage λ of Escherichia coli (Morse et al., 1956; Arber et al., 1957; Campbell, 1957). A summary of the aspects that seem pertinent to studies on bacillus follows. Useful reviews can be found in Campbell (1962, 1971) and Franklin (1971). When the temperate phage λ infects a sensitive host, the linear phage D N A genome enters the cell and cyclizes into a covalently closed double-stranded circle (Fig. 1A). In some infected cells the phage enters the lytic cycle: phage proteins are synthesized, phage DNA is replicated, whole phage particles mature, and the cell lyses to release the new generation of phage. In other infected cells the phage enters the Lysogenic Cycle. A few phage proteins are synthesized, including the proteins called phage repressor and integrase. The phage repressor prevents the tran-scription of most of the phage genome. The integrase catalyzes a site-specific recombination between a particular site (ΡΡ', Fig. 1A) on the phage D N A and a particular site (BET, the attachment site) on the bac-terial chromosome.

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  Mechanisms of Adaptation

  • J.R. Spkatch(Author)
  • 2014(Publication Date)
  • Academic Press

    (Publisher)

  Lysogenic conversion clearly provides a mechanism by which a temperat e phage may be of net benefit to a host. In addition, both transduction by addition and lysogenic con-version provide 4 source of extra DNA for bacteria l or viral evolution. IV. Specific Examples of Bacteriophage Growth A. P HAGE λ— V ARIETY I N L IFE S TYLE 1. G ENERAL O U T L I N E OF P HAGE λ D EVELOPMENT The temperat e phage λ has been the most extensively studied of all bacteriophage , characterized fondly in a biography (Hershey, 1971) and numerous recent review articles (Echols, 1971a, 1972, 1973, 1974; Hersko-witz, 1973; Weisberg et al., 1977). In this section, I will use λ to show how the general framework described in Section III is executed in a particular case. For more details and a more extensive reference list, the reader should consult the review articles noted above. In Section IV,B I will outline the productive growth of the virulent phages Ml 3, T7, and T4. Bacteriophage A is a phage of moderate structura l complexity with an icosahedra l head about 54 nm in diameter and a tail of 150 nm, terminating in a short tail fiber; the genome is a double-strande d D N A molecule of MW 30 χ 10 6 with a 12-base complementary single-stranded region at each 502 HARRISON ECHOLS end that provides for intracellular circularization of the DNA by pairing of these cohesive sites. When λ DNA is injected into a cell, the first events are formation of a molecule and limited transcription of a small region of the λ DNA, princi-pally the Ν and cro genes (Fig. 5). Following this immediat e early period the Ν protein (product of the Ν gene) activates the delayed early stage of viral development in which leftward transcription extends through the recombination genes and rightward transcription is enhanced from the replication genes and extends through gene Q (Echols, 1971b; Thomas, 1971).

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  Biochemistry, International Adaptation

  • Donald Voet, Judith G. Voet(Authors)
  • 2023(Publication Date)
  • Wiley

    (Publisher)

  This explains why poor host nutrition, which results in elevated cAMP concentrations, stimulates lysogenization. Once a prophage has been integrated in the host chro- mosome, lysogeny is stably maintained from generation to generation by λ repressor. This is because λ repressor stimulates its own synthesis at a rate sufficient to maintain lysogeny in the bacterial progeny while repressing the transcription of all other phage genes. In fact, λ repressor t L1 nutL N N 5′ (a) 3′ 3′ 5′ Establishment of lysogeny 5′ (b) 3′ 3′ 5′ Maintenance of lysogeny cII, cIII int p I xis cIII cI p RM o R p R cro nutR t R1 p RE cII ori O P t R2 t R3 Q p R ′ t R ′ qut S cos R b region late genes int xis cIII cI cro cII O P Q S R b region late genes p L o L attP t L1 nutL p I p RM o R p R nutR t R1 p RE ori t R2 t R3 p R ′ t R ′ qut cos p L o L attP Figure 29-43 Control of gene expression in bacteriophage λ. (a) The establishment of lysogeny. (b) The maintenance of lysogeny. The symbols used are described in the legend of Fig. 29-31. [After Arber, W., in Hendrix, R.W., Roberts, J.W., Stahl, F.W., and Weisberg, R.A. (Eds.), Lambda II, p. 389, Cold Spring Harbor Laboratory (1983).] is synthesized in sufficient excess to also repress transcrip- tion from superinfecting λ phage, thereby accounting for the phenomenon of immunity. We shall see below how induction occurs. D. Mechanism of the λ Switch The Lysogenic Cycle is a highly stable mode of phage λ rep- lication; under normal conditions lysogens spontaneously induce only about once per 10 5 cell divisions. Yet, transient exposure to inducing conditions triggers lytic growth in almost every cell of a lysogenic bacterial culture. In this section, we consider how this genetic switch, whose mecha- nism was largely elucidated by Mark Ptashne, can so tightly repress lytic growth and yet remain poised to turn it on efficiently.

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  Mobile Genetic Elements

  • James Shapiro(Author)
  • 2012(Publication Date)
  • Academic Press

    (Publisher)

  In my judgment, the actual data fit much better with the idea that they are deletion derivatives of lambdoid phages. 2. BACTERIOPHAGE λ 95 Β. Distinction between Host Modules and Defective Prophages I have not tried to justify my evaluation of the data on λ-related phages and phage-related DNA segments. These issues have been discussed in more detail elsewhere (Campbell, 1977). However, in the case of phage-related segments, it is important to explain what question is really being asked, and why it seems necessary to ask that question rather than some other one. Most scientists distrust concepts that cannot be translated rather directly into experimental operations. If we ask whether portions of a viral genome can originate from host genes, we might hope to settle the matter by showing that a DNA segment that consists of host genes at the beginning of an experiment can become part of a viral genome during the experiment. However, to define the question in that manner would require us to conclude that viruses originate from host genes every time a lysogenic bacterium is induced, because the genes of the prophage behave as host genes, operationally defined. Few virologists would want to equate induction of a lysogen with the origin of a virus. Because bacteria can become lysogenic in the laboratory by infection, we suspect (although we cannot prove) that most naturally lysogenic bacteria likewise acquired the viral genome through infection. The prophage is therefore treated as a stage in the phage life cycle, rather than as an evolutionary precursor of the phage. To anyone taking the opposite view, the problem of the origin of viruses is of course already solved. Although the distinction just made may appear obvious and trivial, it needs to be stated explicitly before we consider the subject of natural strains carrying defective or incomplete prophages.

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