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The lytic cycle (/ˈlɪtɪk/ LIT-ək), is one of the two cycles of viral reproduction (referring to bacterial viruses or bacteriophages), the other being the lysogenic cycle. The lytic cycle results in the destruction of the infected cell and its membrane. A key difference between the lytic and lysogenic phage cycles is that in the lytic phage, the viral DNA
DNA
exists as a separate molecule within the bacterial cell, and replicates separately from the host bacterial DNA. The location of viral DNA
DNA
in the lysogenic phage cycle is within the host DNA, therefore in both cases the virus/phage replicates using the host DNA
DNA
machinery, but in the lytic phage cycle, the phage is a free floating separate molecule to the host DNA.

Contents

1 Description

1.1 Penetrating 1.2 Gene regulation biochemistry 1.3 Maturation and lysis

2 References

Description[edit] Bacteriophages that only use the lytic cycle are called virulent phages (in contrast to temperate phages). The lytic cycle is a six-stage cycle. In the first stage, called "penetration", the virus injects its own nucleic acid into a host cell. In some viruses this genetic material is circular and mimics a bacterial plasmid. The virus hijacks the cell's replication and translation mechanisms, using them to make more viruses. Once enough virions have accumulated, specialized viral proteins are allowed to dissolve the bacterial cell wall. The cell bursts due to high internal osmotic pressure (water pressure) that can no longer be constrained by the cell wall. This releases progeny virions into the surrounding environment, where they can go on to infect other cells. Penetrating[edit] To infect a cell, a virus must first enter the cell through the plasma membrane and (if present) the cell wall. Viruses do so by either attaching to a receptor on the cell's surface or by simple mechanical force.The binding is due to electrostatic interactions and is influenced by pH and presence of ions such as Mg2+ and Ca2+. The virus then releases its genetic material (either single- or double-stranded RNA
RNA
or DNA) into the cell. In doing this, the cell becomes infected and can also be targeted by the immune system. The virus's nucleic acid uses the host cell’s metabolic machinery to make large amounts of viral components. In the case of DNA
DNA
viruses, the DNA
DNA
transcribes itself into messenger RNA
RNA
(mRNA) molecules that are then used to direct the cell's ribosomes. One of the first polypeptides to be translated destroys the host's DNA. In retroviruses (which inject an RNA
RNA
strand), a unique enzyme called reverse transcriptase transcribes the viral RNA
RNA
into DNA, which is then transcribed again into RNA. Once the viral DNA
DNA
has taken control it induces the host cell's machinery to synthesize viral DNA, protein and starts multiplying. About 25 minutes after initial infection, approximately 200 new bacteriophages are formed and the bacterial cell bursts, i.e. it has undergone lysis. Newly formed phages are released to infect other bacteria and another lytic cycle begins. The phage which causes lysis of the host is called a lytic or virulent phage.[1] The biosynthesis is (e.g. T4) regulated in three phases of mRNA production followed by a phase of protein production.[2]

Early phase Enzymes modify the host's DNA
DNA
replication by RNA
RNA
polymerase. Amongst other modifications, virus T4 changes the sigma factor of the host by producing an anti-sigma factor so that the host promotors are not recognized any more but now recognize T4 middle proteins. For protein synthesis Shine-Dalgarno subsequence GAGG dominates an early genes translation.[3]

Middle phase Virus nucleic acid ( DNA
DNA
or RNA
RNA
depending on virus type).

Late phase Structural proteins including those for the head and the tail.

Gene regulation biochemistry[edit] There are three classes of genes in the phage genome that regulate whether the lytic or lysogenic cycles will emerge. The first are the immediate early genes, the second is the delayed early genes and the third is the late genes. The following refers to the well-studied temperate phage lambda of E. coli.

Immediate early genes: These genes are expressed from promoters recognized by the host RNA
RNA
polymerase. and include cro, cII, and N. CII is a transcription factor that stimulates expression of the main lysogenic repressor gene, cI, whereas Cro is a repressor for cI expression. The lysis-lysogeny decision is mainly influenced by the competition between Cro and CII, resulting in the determination of whether or not sufficient CI repressor is made. If so, CI represses the early promoters and the infection is shunted into the lysogenic pathway. N is an anti-termination factor that is needed for the transcription of the delayed early genes. Delayed early genes: These include the replication genes O and P and also Q, which encodes the anti-terminator responsible for transcription of all the late genes.

Maturation and lysis[edit] Q-mediated turn-on of late transcription begins about 6-8 min after infection, if the lytic pathway is chosen. More than 25 genes are expressed from the single late promoter, resulting in four parallel biosynthetic pathways. Three of the pathways are for production of the three components of the virion: the DNA-filled head, the tail, and the side tail fibers. The virions self-assemble from these components, with the first virion appearing at about 20 min after infection. The fourth pathway is for lysis. In lambda 5 proteins are involved in lysis: the holin and antiholin from gene S, the endolysin from gene R and the spanin proteins from genes Rz and Rz1. In wild-type lambda, lysis occurs at about 50 min, releasing approximately 100 completed virions. The timing of lysis is determined by the holin and antiholin proteins, with the latter inhibiting the former. In overview, the holin protein accumulates in the cytoplasmic membrane until suddenly forming micron-scale holes, which triggers lysis. The endolysin R is released to the periplasm, where it attacks the peptidoglycan. The spanin proteins Rz and Rz1 accumulate in the cytoplasmic and outer membranes, respectively, and form a complex spaning the periplasm through the meshwork of the peptidoglycan. When the endolysin degrades the peptidoglycan, the spanin complexes are liberated and cause disruption of the outer membrane. Destruction of the peptidoglycan by the endolysin and disruption of the outer membrane by the spanin complex are both required for lysis in lambda infections. Lysis
Lysis
inhibition: T4-like phages have two genes, rI and rIII, that inhibit the T4 holin, if the infected cell undergoes super-infection by another T4 (or closely related) virion. Repeated super-infection can cause the T4 infection to continue without lysis for hours, leading to accumulation of virions to levels 10-fold higher than normal. [4] References[edit]

^ bio scholar series ^ Madigan M, Martinko J (editors) (2006). Brock Biology of Microorganisms (11th ed.). Prentice Hall. ISBN 0-13-144329-1. CS1 maint: Extra text: authors list (link) ^ Malys N (2012). " Shine-Dalgarno sequence of bacteriophage T4: GAGG prevails in early genes". Molecular Biology Reports. 39 (1): 33–9. doi:10.1007/s11033-011-0707-4. PMID 21533668.  ^ http://nemetoadreviews.weebly.com/lytic-cyc

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