The tissue‐restricted expression of N‐alpha‐acetyltransferase catalytic subunit gene Arrest Defective 1B in the mouse and human is regulated by CpG island methylation

N‐alpha‐terminal protein acetylation is one of the most common modification processes occurring on eukaryotic proteins. Arrest Defective 1B ( ARD1B , also known as NAA11 ), the functional retrocopy of the catalytic subunit of N‐alpha‐ acetyltransferase, is expressed predominantly in the testis. We found that the expression of ARD1B in mouse spermatogenic cells and tissues correlated with the CpG island methylation pattern of the gene. Subsequent analyses, which include promoter assay, in vitro methylation assay and 5‐aza‐2′‐deoxycytidine treatment, further confirm the role of DNA methylation in controlling ARD1B expression. We demonstrated that a similar mechanism for regulation of expression of orthologous ARD1B occurs in human cells. The restricted expression pattern of ARD1B is regulated by an evolutionarily conserved mechanism that involves CpG island methylation. This research is supported by the Intramural Research Program of Eunice Kennedy Shriver National Institute of Child Health and Human Development, National Institutes of Health.