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

Tuesday, October 25, 2011 — Poster Session II
Noon – 2:00 p.m.	Natcher Conference Center	NICHD	EPIGEN/TRANS/CHROM-9

Authors

• ALY Pang
• J Clark
• J Fang
• WY Chan
• OM Rennert

Abstract

N(alpha)-acetylation is one of the most common modification processes occurring on eukaryotic proteins. Arrest Defective 1B (Ard1b, now known as Naa11), the functional retrocopy of the catalytic subunit of N(alpha)-acetyltransferase NatA, 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. The expression of the orthologous ARD1B (now known as NAA11) is also tissue-specific and regulated by a similar mechanism in human cells. Our data suggest that the regulatory mechanism of the transcription of Ard1b/ARD1B is evolutionarily conserved and involves CpG island methylation.

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