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DRD1‐Pol V‐dependent self‐silencing of an exogenous silencer restricts the non‐cell autonomous silencing of an endogenous target gene
Author(s) -
Dong Li,
Liu Meng,
Fang YuanYuan,
Zhao JianHua,
He XiangFeng,
Ying XiaoBao,
Zhang YiYue,
Xie Qi,
Chua NamHai,
Guo HuiShan
Publication year - 2011
Publication title -
the plant journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.058
H-Index - 269
eISSN - 1365-313X
pISSN - 0960-7412
DOI - 10.1111/j.1365-313x.2011.04714.x
Subject(s) - gene silencing , biology , silencer , microbiology and biotechnology , methylation , rna silencing , endogeny , dna methylation , rna induced silencing complex , transgene , rna interference , gene , genetics , gene expression , rna , mechanical engineering , engineering , inlet , endocrinology
Summary In plants, the exogenous transgene transcribing inverted‐repeat (exo‐ IR ) sequences produces double‐stranded RNAs that are processed by DCL4. The 21‐nt small interfering RNAs generated function as mobile signals to trigger non‐cell autonomous silencing of target endogenes in the neighboring 10–15 cells. The potential involvement of nuclear silencing pathway components in signal spreading or sensing in target cells is not clear. Here, we demonstrate that the exo‐ IR silencer (exo‐ Pdsi ) is negatively autoregulated through methylation spreading, which acts in cis to reinforce the self‐silencing of the silencer. Mutations affecting nuclear proteins DRD1 and Pol V (NRPE1 or NRPD2) relieved exo‐ Pdsi self‐silencing, resulting in higher levels of Pdsi transcripts, which increased the non‐cell autonomous silencing of endo‐ PDS . Our results suggest that in an experimental silencing pathway, methylation spreading on a silencer transgene may not have a direct endogenous plant counterpart when the protein‐encoding gene is the target. DRD1‐Pol V‐dependent de novo methylation, by acting in cis to reinforce self‐silencing of exo‐ IR , may play a role in restraining the inappropriate silencing of active protein‐coding genes in plants.