The developmentally regulated RNA-binding protein Lin28 blocks processing of let-7 family microRNAs (miRNAs) in embryonic cells. The molecular basis for this selective miRNA processing block is unknown. Here we find that Lin28 selectively binds the terminal loop region of let-7 precursors in vitro and that the loop mediates miRNA processing inhibition in vivo. Additionally, we identify the doma...

The current study investigated the possible effects of static magnetic fields (SMFs) on the developmental and aging processes of Caenorhabditis elegans. Nematodes were grown in the presence of SMFs of strengths varying from 0 to 200 mT. The rate of development and the lifespan were recorded. Treatment with a 200 mT SMF reduced the development time from the L2 to the L3 stage by 20%, from L3 to ...

Single-molecule techniques have been used for only a subset of biological problems because of difficulties in studying proteins that require cofactors or post-translational modifications. Here, we present a new method integrating single-molecule fluorescence microscopy and immunopurification to study protein complexes. We used this method to investigate Lin28-mediated microRNA uridylation by TU...

The first microRNAs were identified in Caenorhabditis elegans based on their functions in the temporal regulation of stage-specific cell fate decisions. Until now, it was not known whether the so-called heterochronic genes that encode miRNAs are also involved in controlling developmental transitions in other organisms. New findings by Sokol et al. (this issue of Genes & Development, pp. 1591-15...

The mechanisms of gene expression regulation by miRNAs have been extensively studied. However, the regulation of miRNA function and decay has long remained enigmatic. Only recently, 3' uridylation via LIN28A-TUT4/7 has been recognized as an essential component controlling the biogenesis of let-7 miRNAs in stem cells. Although uridylation has been generally implicated in miRNA degradation, the n...

Like mammalian neurons, Caenorhabditis elegans neurons lose axon regeneration ability as they age, but it is not known why. Here, we report that let-7 contributes to a developmental decline in anterior ventral microtubule (AVM) axon regeneration. In older AVM axons, let-7 inhibits regeneration by down-regulating LIN-41, an important AVM axon regeneration-promoting factor. Whereas let-7 inhibits...