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As the founding member of the microRNA (miRNA) gene family, insights into  lin-4  regulation and function have laid a conceptual foundation for countless miRNA-related studies that followed. We previously showed that a transcriptional  lin-4  reporter in  C .  elegans  was positively regulated by a  lin-4 -complementary element (LCE), and by  lin-4  itself. In this study, we sought to (1) identify additional factors required for  lin-4  reporter expression, and (2) validate the endogenous relevance of a potential positive autoregulatory mechanism of  lin-4  expression. We report that all four core nuclear RNAi factors ( nrde-1 ,  nrde-2 ,  nrde-3  and  nrde-4 ), positively regulate  lin-4  reporter expression. In contrast, endogenous  lin-4  levels were largely unaffected in  nrde-2;nrde-3  mutants. Further, an endogenous LCE deletion generated by CRISPR-Cas9 revealed that the LCE was also not necessary for the activity of the endogenous  lin-4  promoter. Finally, mutations in mature  lin-4  did not reduce primary  lin-4  transcript levels. Taken together, these data indicate that under growth conditions that reveal effects at the transgenic locus, a direct, positive autoregulatory mechanism of  lin-4  expression does not occur in the context of the endogenous  lin-4  locus.

lin-4 and the NRDE pathway are required to activate a transgenic lin-4 reporter but not the endogenous lin-4 locus in C. elegans