Questions: Bacteriophage Lytic and Lysogenic Cycles

Question 1

A harmless E. coli laboratory strain is infected by a temperate phage carrying a toxin gene. The bacteria survive, show no signs of phage activity, and divide normally. Six months later, descendants of these bacteria are found to produce a potent toxin. What is the most likely explanation?

• A. The phage repeatedly reinfected each generation of bacteria, gradually inserting the toxin gene more stably over time
• B. The toxin gene mutated into the bacterial chromosome spontaneously, triggered by the initial phage infection
• C. The phage integrated into the bacterial chromosome as a prophage (lysogeny), and the toxin gene was expressed as part of lysogenic conversion, inherited by all daughter cells
• D. Viral DNA causes spontaneous mutations that occasionally generate toxin-producing variants after long incubation periods

Answer: (C)

This is lysogeny followed by lysogenic conversion. The phage integrated into the bacterial chromosome as a prophage — silenced by CI repressor — and has been replicated passively with every cell division for six months. The toxin gene carried by the prophage is now expressed as part of the bacterial genome, a process called lysogenic conversion. Every daughter cell inherits both the prophage and its toxin-encoding genes. This is exactly how harmless bacteria become dangerous pathogens: diphtheria toxin, cholera toxin, and Shiga toxin are all prophage-encoded.

Question 2

A population of lysogenic bacteria carrying lambda prophage is exposed to UV radiation. What is the most likely outcome?

• A. The prophage remains dormant because UV radiation damages bacterial DNA but cannot affect integrated phage DNA
• B. UV permanently eliminates the prophage by causing double-strand breaks in the bacterial chromosome at the integration site
• C. The prophage becomes more stably integrated as the bacteria mount a stress response protecting chromosomal DNA
• D. UV triggers the bacterial SOS response, which degrades CI repressor, inducing the prophage to excise and enter the lytic cycle

Answer: (D)

UV radiation causes DNA damage that activates the SOS response — the bacterial emergency repair system. A key SOS component, RecA, becomes activated and cleaves the CI repressor protein that was keeping all lytic genes silenced. Without CI repressor, lytic genes are derepressed: the prophage excises from the chromosome and initiates the lytic cycle, producing hundreds of new phages and lysing the cell. This induction is adaptive for the phage: a damaged host is a poor long-term host, so the phage abandons ship to find healthier bacteria.

Question 3

Prophage DNA is replicated passively along with the host bacterial chromosome at every cell division, allowing the phage genome to persist across generations without producing any phage particles.

• T. True
• F. False

Answer: True

True. This is the defining feature of lysogeny. The prophage is treated as just another segment of the bacterial chromosome by the host's replication machinery. CI repressor silences all lytic and structural genes, so no phage proteins are made and no particles are assembled. The prophage hitches a free ride, copied faithfully into every daughter cell, potentially for thousands of generations — until induction triggers excision and the lytic cycle.

Question 4

Virulent phages like T4 can choose between lytic and lysogenic cycles depending on host cell conditions, just like temperate phages.

• T. True
• F. False

Answer: False

False. Virulent phages are obligate lytic killers — they lack the genetic machinery (CI repressor, integration systems like integrase and attP/attB sites) required for lysogeny. Once a virulent phage infects a bacterium, it always proceeds through the lytic cycle and kills the host. Only temperate phages have the regulatory circuitry to 'decide' between lytic and lysogenic outcomes based on environmental conditions (host nutritional state, multiplicity of infection, etc.). This is a fundamental distinction between the two types.

Question 5

Why is lysogenic conversion medically significant? Use a specific example to illustrate why understanding this process matters for bacterial pathogenesis.

Model answer: Lysogenic conversion is the process by which a prophage's genes alter the phenotype of its bacterial host, often in ways that directly affect virulence. Medically, this means that a completely harmless bacterial strain can be transformed into a deadly pathogen by a single phage infection event — without any mutation in the bacterium's own genome. For example, Vibrio cholerae strains without a specific prophage (CTXφ) are non-pathogenic; infection by CTXφ introduces the cholera toxin gene as part of the prophage, and lysogenic conversion makes the bacterium capable of causing epidemic cholera. Similarly, Corynebacterium diphtheriae is harmless without its prophage, which carries the diphtheria toxin gene. This matters because it explains how new pathogenic strains can emerge suddenly, why antibiotic-treated patients can sometimes worsen (inducing lytic cycles releases more toxin), and why virulence cannot always be predicted from bacterial genome sequence alone — the phage is the missing piece.

The concept challenges the assumption that a bacterium's danger is fixed by its own genome. Prophages are mobile genetic elements that can be acquired, transferred between strains, and induced — making them dynamic determinants of pathogenicity rather than static features.