Drug‐induced hypomethylation of a posttranscriptionally silenced transgene locus of tobacco leads to partial release of silencing

FEBS Letters

Kovařı́k, Ales¹  Depicker, Anna²  Van Houdt, Helena²  Holý, Antonı́n³ 

[1] Institute of Biophysics, Academy of Sciences of the Czech Republic, Královopolská 135, 612 65 Brno, Czech Republic;Department of Molecular and Plant Genetics, Flanders Interuniversity Institute for Biotechnology, University of Gent, K.L. Ledeganckstraat 35, B-9000 Gent, Belgium;Institute of Organic Chemistry and Biochemistry, Academy of Sciences of the Czech Republic, Flemingovo nám. 2, 166 10 Prague 6, Czech Republic

关键词: DNA methylation;    Gene silencing;    Hypomethylation drug;    T-DNA;    Tobacco;    DHPA;    dihydroxypropyladenine;    ELISA;    enzyme-linked immunosorbent assay;    HElo1;    hemizygous for locus 1;    HElo2;    hemizygous for locus 2;    HElo1/HElo2;    hybrid of HElo1 and HElo2;    NPTII;    neomycin phosphotransferase II;    PTGS;    posttranscriptional gene silencing;   

DOI  :  10.1016/S0014-5793(00)01077-2

学科分类：生物化学/生物物理

来源: John Wiley & Sons Ltd.

【 摘 要 】

The effect of DNA methylation upon posttranscriptional gene silencing (PTGS) has been investigated in transgenic tobacco lines showing PTGS and methylation of the neomycin phosphotransferase II (nptII) reporter genes. Application of the hypomethylation drugs dihydroxypropyladenine or 5-azacytidine resulted in approximately 30% reduced methylation of cytosines located in a non-symmetrical context in the 3′ untranslated region of the nptII transgenes. The hypomethylation was accompanied by up to 12-fold increase in NPTII protein levels, suggesting that methylation of non-symmetrical motifs may account for an increased degree of PTGS. Models for the possible role of DNA methylation in PTGS are discussed.

【 授权许可】

Unknown