Small RNAs in tgh-1 mutant

miRNAs are regulators of gene expression in plants and animals. Their biogenesis is precisely controlled to secure normal development of organisms. Here we report that TOUGH (TGH) is a novel component of DCL1-HYL1-SE complex that processes of primary transcripts of miRNAs (pri-miRNAs) into miRNAs in Arabidopsis. Lack of TGH impairs multiple DCL activities in vitro and reduces the accumulation of miRNAs and siRNAs in vivo. TGH is an RNA binding protein, binds with pri-miRNAs in vivo and contributes to pri-miRNA-HYL1interaction. These results indicate that TGH might regulate abundance of miRNAs through promoting the DCL1 cleavage efficiency and/or recruitment of pri-miRNAs. Because TGH is a conserved protein in plants and animals, our study shall have implications on miRNA pathway in other organisms Overall design: tgh-1 mutant vs. wild type