Conserved DNA methylation in Gadd45a(-/-) mice.
Gadd45a (growth arrest and DNA-damage-inducible protein 45 alpha) plays a pivotal role in cellular stress responses and is implicated in DNA repair, cell cycle arrest and apoptosis.(1) Recently, it was proposed that GADD45A is a key regulator of active DNA demethylation by way of its role in DNA repair.(2) Barreto et al. reported that Gadd45a overexpression activated transcription from methylation-silenced reporter plasmids and promoted global DNA demethylation. siRNA-mediated knockdown of Gadd45a levels resulted in increased levels of DNA methylation at specific endogenous loci. Based on these exciting results, Gadd45a(-/-) mice might be predicted to have a hypermethylation phenotype. We report here that neither global nor locus-specific methylation is increased in Gadd45a(-/-) mice.
Engel
Nora
N
Fels Institute for Cancer Research & Molecular Biology, Temple University School of Medicine, Philadelphia, PA 19140, USA. noraengel@temple.edu
Tront
Jennifer S
JS
Erinle
Toyin
T
Nguyen
Nghi
N
Latham
Keith E
KE
Sapienza
Carmen
C
Hoffman
Barbara
B
Liebermann
Dan A
DA
D000818:Animals; D018797:Cell Cycle Proteins; D019175:DNA Methylation / Q000187:drug effects; D004260:DNA Repair; D051379:Mice; D018345:Mice, Knockout; D009687:Nuclear Proteins / Q000172:deficiency*; D034741:RNA, Small Interfering / Q000494:pharmacology; D000097642:GADD45 Proteins
D018797:Cell Cycle Proteins; D009687:Nuclear Proteins; D034741:RNA, Small Interfering; C499072:Gadd45a protein, mouse; D000097642:GADD45 Proteins