Microbiology MCAT Practice Question
A 34-year-old male presents to the clinic with recurrent skin infections caused by Staphylococcus aureus. His medical history is notable for multiple episodes of severe cellulitis over the past 2 years. Genetic testing reveals a deficiency in RecA protein function due to a loss-of-function mutation. Laboratory analysis of S. aureus isolates obtained from this patient demonstrates that the bacteria are lysogenically infected with a temperate bacteriophage carrying virulence genes (including exotoxin A). When these lysogenic bacteria are exposed to UV radiation in vitro, they fail to undergo phage induction despite DNA damage. Which of the following best explains why these lysogenic bacteria cannot mount a typical phage-mediated lytic response to UV damage?
Answer choices
- ARecA protein normally enhances CI repressor synthesis, so its absence prevents increased repressor production needed for lytic cycle initiation
- BRecA protein facilitates CI repressor self-cleavage in response to SOS activation, allowing derepression of lytic genes; without functional RecA, CI repressor remains bound to operators and blocks lytic gene expressionCorrect answer
- CRecA protein is required for integration of additional prophage copies into the bacterial chromosome, which is necessary for phage induction
- DThe SOS response cannot be activated without RecA protein, preventing any cellular response to DNA damage and thus maintaining lysogeny by default
- ERecA protein normally degrades Cro protein, which would otherwise prevent CI repressor from binding to operators; loss of RecA results in unopposed Cro activity
- FRecA protein directly binds to operator sequences OR and OL, competing with CI repressor for these sites; without RecA, CI repressor binds more tightly and prevents lytic gene induction
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