Molecular control of replication licensing speed by c-MYC

c-MYC potently accelerates genome-wide origin licensing in G1, separating rapid licensing from its gene-expression function, with licensing speed increased via chromatin changes.

• Why it matters: Short G1 phases require faster origin licensing to avoid incomplete replication and genome instability, but the mechanisms that speed licensing were largely unclear.
• What they did: Using quantitative single-cell approaches, the study shows c-MYC accelerates licensing through TRRAP and GCN5 and induces widespread linker histone H1 eviction; reducing chromatin-bound H1 also speeds licensing, including in heterochromatin.
• The result: Global chromatin opening linked to c-MYC is sufficient to accelerate licensing when G1 is short, suggesting relevance to early development, rapid progenitor proliferation, and adaptation to oncogene activation.

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