High impact information on lin-41

• Here, we report that in C. elegans, regulation by the let-7 miRNA results in degradation of its lin-41 target mRNA, despite the fact that its 3'UTR regulatory sequences can only partially base-pair with the miRNA [1].
• A reporter gene bearing the lin-41 3' untranslated region is temporally regulated in a let-7-dependent manner [2].
• Furthermore, a combination of phenotypic abnormalities and RNA analysis suggests a role for dcr-1 in a regulatory pathway comprised of small temporal RNA (let-7) and its target (e.g., lin-41) [3].
• A lin-41::GFP fusion gene is downregulated in the tissues affected by lin-41 at the time that the let-7 regulatory RNA is upregulated [4].
• Novel gain-of-function alleles demonstrate a role for the heterochronic gene lin-41 in C. elegans male tail tip morphogenesis [5].

Biological context of lin-41

• C. elegans lin-41 is one of the RBCC-NHL families and the predicted amino acid sequences of isolated two genes encode the same family proteins [6].
• Reciprocal expression of lin-41 and the microRNAs let-7 and mir-125 during mouse embryogenesis [7].
• RNA containing the lin-41 3' UTR and an iron response element in the 5' UTR sedimented with polysomes when cells were incubated with iron, but showed ribosome run-off when the iron was chelated [8].

Other interactions of lin-41

• Like lin-41 mutations, hbl-1 loss-of-function partially suppresses a let-7 mutation [9].
• Using luciferase assay, we showed that lin-41 expression can be regulated through let-7 complementary sites [6].

References