The FERONIA-YUELAO module functions in translation by regulating the abundance of tRNA fragments

tRNA fragments(tRFs)are a recently identified class of small noncoding RNAs. To date, the abundance pathway and functional mechanisms of tRFs in plants are largely unclear. Here, we investigated the mechanism by which the Arabidopsis thaliana receptor kinase FERONIA (FER) regulates the abundance of tRFs to inhibit global mRNA translation, including the well-identified FER pathway members ROPs translation. We demonstrate that FER regulates the abundance of tRFs by directly phosphorylating a novel type of tRNA-binding protein YUELAO (YL) to modulate YLs function. The downregulation of FER and YL prevented the modification of tRNA e.g. cytosine-5-methylation (m5C) and 2-O-methylation (Cm),thereby increasing tRF abundance. Furthermore, we show that YL acts as an important genetical downstream target of FER signaling, and knockdown of the specific tRF partially rescues FER and YL mutants root hair growth defects. Our findings shed light on the abundance and regulatory mechanisms of tRF and their role in inhibiting translation in plants.