= Solution
<aphidicolin> increases the abnormal-locus fraction from roughly 40% to about 55–60% in all three lines. \b[Inhibition of replicative <DNA polymerases> increases <replication stress> at an intrinsically difficult-to-complete region.] Tandem repeats can complicate fork progression or <chromosome> organization. Slower or incomplete synthesis leaves <underreplicated DNA>, unresolved replication intermediates or abnormal condensation as <biological cells> approach <mitosis>; these can appear as split signals or gaps and can predispose to actual breakage.
This is an increase of approximately 15–20 percentage points, not proof of a 15–20-fold change. The two independent measurements per condition support a reproducible direction, but the graph does not provide enough information for a precise significance calculation or a quantitative model of fork failure. <aphidicolin> need not bind NVNA1 or the repeat sequence directly. Because these are uninfected <biological cells>, the result establishes susceptibility of the host locus to <replication stress> independently of viral <protein> expression.
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