Volume 20, number 4, p. 1134–1139, 2000. Since publication of this article, we found that the acetyl coenzyme A binding site TAFII250 mutant contained the ts13 mutation (G716D) as well as the reported G992D, G994D mutations. The presence of the ts13 mutation had been unintentionally introduced during the mutagenesis process. Since the ts13 TAFII250 mutant has a defect in histone acetyltransferase (HAT) activity (see Fig. 1) and fails to rescue the transcriptional and proliferative defect in ts13 cells, we suspected that our results might be attributed solely to the presence of the ts13 (G716D) mutation. We therefore generated the correct acetyl coenzyme A binding site mutations and found that the G992D and G994D mutations alone do not compromise TAFII250 HAT activity. In addition, the acetyl coenzyme A mutant is fully capable of rescuing ts13 cells from cell cycle arrest and restoring transcription to the cyclin D1 promoter at 39.5°C.
Although these findings differ from our published results, they do not contradict or disprove our hypothesis that TAFII250 HAT activity is necessary for the G1/S transition. We regret our error and apologize for any confusion it may have caused.