GSE66986
Novel DICER-LIKE1 siRNAs Bypass the Requirement for DICER-LIKE4 in Maize Development
Dicer enzymes function at the core of RNA silencing to defend against exogenous RNA, or as an endogenous mechanism of gene regulation. Plant DICER-LIKE4 (DCL4) performs dual functions, acting in antiviral defense, as well as in development via the biogenesis of tasiR-ARFs. These small RNAs play an essential role in the grasses and act to spatially define the expression domain of AUXIN RESPONSE FACTOR3 (ARF3) transcription factors. However, contrary to tasiR-ARFs’ essential function in development, DCL4 proteins exhibit strong evidence of recurrent adaptation typical of host factors involved in antiviral immunity. Here, we address how DCL4 balances its role in development with pressures to diversify in response to viral attack. We show that, in contrast to other tasiR-ARF biogenesis mutants, dcl4 null alleles condition an uncharacteristically mild phenotype, correlated with normal expression of select arf3 targets. Loss of DCL4 activity yields a class of 22-nt tasiR-ARF variants associated with the processing of arf3 transcripts into 22-nt secondary siRNAs by DCL1. Our findings uncover the presence of a novel DCL1-dependent siRNA pathway that bypasses the otherwise adverse developmental effects of DCL4 mutations. This novel pathway is predicted to have important implications for DCL4’s role in antiviral defense by reducing the selective constraints on DCL4 and allowing it to diversify in response to viral suppressors. Overall design: Examination of small RNAs isolated from dcl4, dcl1 and double mutants in imbibed kernels of maize