Ago1 is Required for RNA-mediated gene silencing (RNAi) . Binds to short RNAs such as microRNAs (miRNAs) or short interfering RNAs (siRNAs), and represses the translation of mRNAs which are complementary to them.This is in Human.
I think its also required for transcriptional gene silencing (TGS) of promoter regions which are complementary to bound short antigene RNAs (agRNAs). its said that Ago protein guides the agRNA to its promoter target, which can be non-coding transcript overlapping the promoter or the chromosomal DNA. Ago proteins then recruits histone modifying enzymes such as histone methyltransferase to the promoter to activate transcription by causing permissive epigenetic changes.
am not quite clear about your query. this is what i have read about Ago proteins.
Thanks for this useful link. I am going through the link sent.
My basic idea is that are their any natural cases of tsg reported with connection to other sources of naturally found small RNA like miRNA (the ones which get imported to nucleus) or the dsRNA viruses which their marks in
search for siRNA interactions in plants rather than in animals as you know miRNAs processing in animals takes place outside the nucleus. In plants the processing of mature miRNA is done by DCL1 inside the nucleus therefore you may find the more resources and/or experiments in plants . Try searching in GEO (www.ncbi.nlm.nih.gov/geo/) or SRA for NGS or other related data and experiments.
I don't know about miRNA but I noticed in a transcriptomic study of the silencing effect of siRNA that most of the down regulated genes had homology at the DNA but not on the mRNA level. Further studies will be of course needed to make conclusive statement.
Thank you Dr Dever. I find this very interesting. I had heard about lmiRNA before I guess but never read much of citations. It will be great if you can send me some cited refereces of this pathway. DCL3 splicing and loading of AGO4 is a new concept. But the question is that is the phenomenon evoking epigenetic changes as it happens in TGS led by siRNA antisense strand.