摘要
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Summary
HEN1-mediated 2鈥?<em>Oem>-methylation has been shown to be聽a key聽mechanism to protect plant microRNAs (miRNAs) and small interfering RNAs (siRNAs) as well as animal piwi-interacting RNAs (piRNAs) from degradation and 3鈥?terminal uridylation []. However, enzymes uridylating unmethylated miRNAs, siRNAs, or piRNAs in <em>hen1em> are unknown. In this study,聽a genetic screen identified a second-site mutation <em>hen1 suppressor1-2em> (<em>heso1-2em>) that partially suppresses the morphological phenotypes of the hypomorphic <em>hen1-2em> allele and the null <em>hen1-1em> allele in <em>Arabidopsisem>. <em>HESO1em> encodes a terminal nucleotidyl transferase that prefers to add untemplated uridine to the 3鈥?end of RNA, which is completely abolished by 2鈥?<em>Oem>-methylation. <em>heso1-2em> affects the profile of u-tailed miRNAs and siRNAs and increases the abundance of truncated and/or normal sized ones in <em>hen1em>, which often results in increased total amount of miRNAs and siRNAs in <em>hen1em>. In contrast, overexpressing <em>HESO1em> in <em>hen1-2em> causes more severe morphological defects and less accumulation of miRNAs. These results demonstrate that HESO1 is an enzyme uridylating unmethylated miRNAs and siRNAs in <em>hen1em>. These observations also聽suggest that uridylation may destabilize unmethylated miRNAs through an unknown mechanism and compete with 3鈥?to-5鈥?exoribonuclease activities in <em>hen1em>. This study shall have implications on piRNA uridylation in <em>hen1em> in animals.
