= Solution
With <nucleosomes> alone, neither competitor substantially removes the main <nucleosome> band, although some free labelled <DNA> is present. With nucleosome–NVNA1 complexes, increasing <specific competitor DNA> removes the extra shifts and restores the <nucleosome> band. \b[The starting shifted complexes therefore contained <histones> as well as NVNA1:] competitor recognition sites draw NVNA1 away while leaving labelled <DNA> associated with <histones>.
<nonspecific competitor DNA> gives a different endpoint. The shifted population changes to a band matching the far-right NVNA1–naked-DNA control, rather than returning mainly to the <nucleosome> position. The labelled <DNA> remains bound to NVNA1 while <histones> can transfer to the excess competitor <DNA>. \b[NVNA1 binding destabilizes the <nucleosome> against competitor-induced <histone> displacement.] Remaining shifted <DNA> is not evidence that the <histone octamer> remained: its mobility must be compared with both controls. The nucleosome-only competition lanes show that competitor <DNA> alone is insufficient to cause the same conversion. Histone-specific detection would confirm the inferred component loss. A closely analogous ternary-complex and competition analysis was demonstrated for EBNA1; it provides a methodological precedent without establishing the identity of NV.<Epstein–Barr nuclear antigen 1 binds and destabilizes nucleosomes at the viral origin of latent DNA replication by Tina M. Avolio-Hunter and others>[Figures 2–4: ternary complexes, specific competition and histone displacement]{ref}
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