| Evidence type | Key finding | Quantitative/statistical details | Source (include DOI URL and year) | Notes/limitations |
|---|---|---|---|---|
| Phenotype/genetics | Mutations in T4 **ac** (gene 52.2) confer resistance to acriflavin, enabling phage development under acriflavin selection (AcS→AcR assay). | Forward mutation rate to AcR increased in **mutA** host cells by about **4–10-fold** versus parental cells. Example rates shown for two T4 backgrounds: **3 to 28 ×10^-8** and **4.7 to 50 ×10^-8**; **5.5 to 22 ×10^-8** and **4.4 to 17 ×10^-8** (pqac-00000004) | Mamun et al., *Molecular Microbiology* (2006). DOI: https://doi.org/10.1111/j.1365-2958.2006.05490.x (2006) (pqac-00000000, pqac-00000004) | The paper explicitly states that the **mode of action and function remain unknown**; the assay reports selectable phenotype, not biochemical mechanism. |
| Sequence/features | The **ac** gene is a very small target used for mutagenesis studies. | Gene length is **156 bp**; the **termination codon is at positions 154–156** (pqac-00000005) | Mamun et al., *Molecular Microbiology* (2006). DOI: https://doi.org/10.1111/j.1365-2958.2006.05490.x (2006) (pqac-00000000, pqac-00000001, pqac-00000005) | Small gene size makes it useful for forward-mutation analysis, but also means functional/domain inference from sequence alone is limited in this paper. |
| Sequence/features / mutation spectrum | In **mutA** cells, the **ac** mutation spectrum shifts strongly toward insertions, especially 1-bp A:T insertions and repeat-associated events. | Insertions:deletions ratio changes from about **1:1 in wild type** to **3:1 in mutA**; **1-bp A:T insertions** rise about **33-fold**; **insertions within repeats** rise about **32-fold**; A:T-targeted substitutions appear elevated about **24-fold** (pqac-00000005) | Mamun et al., *Molecular Microbiology* (2006). DOI: https://doi.org/10.1111/j.1365-2958.2006.05490.x (2006) (pqac-00000001, pqac-00000005, pqac-00000006, pqac-00000007) | About half of sequenced AcR mutants carried changes within **ac** itself (**68/126** in WT; **68/120** in mutA), implying some AcR mutants map outside **ac** or were otherwise unresolved. |
| Genomic context | Plasmid mapping places **ac** in the T4 genomic region near the **rII** locus and **gene 52**. | In plasmid **pTB401** (~**1,100 bp** insert), the mapped order includes **... stp r ac gene52**; the insert carries the **saA9** deletion. The mapped region spans parts of **rIIB** and **52** and places **ac** adjacent to gene 52 (pqac-00000003) | Selzer et al., *Molecular and General Genetics MGG* (published in tool record as 2004; original classic study). DOI: https://doi.org/10.1007/bf00268772 (tool record year 2004) (pqac-00000002, pqac-00000003) | This is **mapping/context evidence**, not direct functional characterization of ac protein 52.2. |
| Phenotype/genetics / interpretation | **ac** is valuable as a reporter for T4 replication fidelity in host mutator backgrounds. | In the AcS→AcR assay, average mutation rates for sequenced **ac** mutants were summarized as **2.1 ×10^-8** (WT) versus **22 ×10^-8** (**mutA**) (pqac-00000005) | Mamun et al., *Molecular Microbiology* (2006). DOI: https://doi.org/10.1111/j.1365-2958.2006.05490.x (2006) (pqac-00000005) | These data support use of **ac** as a mutational readout, but they do **not** establish whether ac is enzymatic, structural, or regulatory in normal T4 biology. |


*Table: This table condenses the directly supported evidence recovered for bacteriophage T4 gene ac/protein 52.2 (UniProt P18924). It highlights the strongest experimentally grounded findings on phenotype, sequence features, mutation statistics, and genomic context while making clear where functional knowledge remains limited.*