德國最新研究發(fā)現(xiàn),，脫氧核糖核酸（DNA）的兩種酶會互相爭奪對基因表達的“控制權”，這種爭奪會導致DNA上的基因編碼讀取出錯,，從而引發(fā)相關疾病,。
德國杜伊斯堡－埃森大學日前發(fā)表公報說，該校研究人員發(fā)現(xiàn)名為Sir2的酶和名為Rpd3的酶會互相爭奪對基因表達的“控制權”,。當其中一種酶過度活躍,，另一種酶的作用則會減弱，造成基因表達失去平衡,，DNA上的基因編碼讀取出現(xiàn)錯誤,，從而引發(fā)相關疾病。
研究人員表示,，將進一步研究這兩種酶相互作用的具體機理,，以便有助于研究由此引發(fā)的相關疾病。
這一成果發(fā)表在最新一期美國《國家科學院學報》上,。（生物谷Bioon.com）
生物谷推薦原始出處：
PNAS January 19, 2010, doi: 10.1073/pnas.0909169107
Rpd3-dependent boundary formation at telomeres by removal of Sir2 substrate
Stefan Ehrentrauta, Jan M. Webera, J. Nikolaj Dybowskib, Daniel Hoffmannb, and Ann E. Ehrenhofer-Murraya,1
a Abteilung für Genetik and
bAbteilung für Bioinformatik, Zentrum für Medizinische Biotechnologie (ZMB), Universit?t Duisburg-Essen, D- 45117 Essen, Germany
Boundaries between euchromatic and heterochromatic regions until now have been associated with chromatin-opening activities. Here, we identified an unexpected role for histone deacetylation in this process. Significantly, the histone deacetylase (HDAC) Rpd3 was necessary for boundary formation in Saccharomyces cerevisiae. rpd3? led to silent information regulator (SIR) spreading and repression of subtelomeric genes. In the absence of a known boundary factor, the histone acetyltransferase complex SAS-I, rpd3? caused inappropriate SIR spreading that was lethal to yeast cells. Notably, Rpd3 was capable of creating a boundary when targeted to heterochromatin. Our data suggest a mechanism for boundary formation whereby histone deacetylation by Rpd3 removes the substrate for the HDAC Sir2, so that Sir2 no longer can produce O-acetyl-ADP ribose (OAADPR) by consumption of NAD+ in the deacetylation reaction. In essence, OAADPR therefore is unavailable for binding to Sir3, preventing SIR propagation.
