Because functional AREs normally contain clustered repeats of the characteristic AUUUA motif, cooperative binding of several factors in close proximity has been proposed. Small non-coding RNAs such as microRNAs and short MG132 interfering RNAs also lead to the destabilization and translational repression of cognate mRNAs. They are bound by proteins of the Argonaute family and confer target mRNA specificity to the RNA-induced silencing complex. Based on data obtained in Drosophila and human cell cultures, Jing et al. proposed that miRNAs with appropriate sequence complementarity can recruit RISC to the ARE and thus mediate part of the repressive effect. In another report, Vasudevan and Steitz demonstrated that recognition of an ARE by miRNAloaded RISC, in association with the Fragile-X mental retardation-related protein 1, activates mRNA translation in quiescent cells. This is surprising given that AREs and miRNAs are both generally regarded as negative regulators. Cross-talk between the miRNA and the ARE pathway has also been observed in liver cells. When grown under normal conditions, CAT-1 mRNA is targeted by miR-122, leading to its re-localization into P-bodies and translational suppression. Upon amino acid starvation, the ARE-binding HuR protein is translocated into the cytoplasm and recruited to an ARE in the CAT-1 mRNA, downstream of the miR-122 binding site. Recruitment of HuR causes miR-122 to dissociate, whereby CAT-1 mRNA is released from P-bodies and resumes translation. While most work on ARE-mediated regulation has been performed in mammalian systems, it has become clear that Drosophila melanogaster is not only capable of recognizing and degrading mRNAs containing mammalian AREs, but also uses this system to control endogenous transcripts, e.g. the mRNA coding for the antimicrobial peptide cecropin A1. Moreover, the TTP-homolog tis-11 was found to be essential for this regulation in Drosophila and overexpression of tis-11 results in a further increase of the mRNA degradation rate. We revisited the proposal by Jing et al. that miRNAs are required for degradation of ARE-containing mRNAs. To this end, we examined AU-rich element mediated decay in mouse embryonic fibroblasts lacking the essential miRNA biogenesis factor dicer, and found that the half-life of endogenously expressed ier3 mRNA, an ARE-containing transcript, is unchanged. In cultured Drosophila S2 cells we observed that ARE-containing reporter mRNAs as well as endogenous cecA1 mRNA are repressed in a tis-11 dependent manner. Again, this repression did not depend on components of the miRNA or siRNA pathways. Direct inhibition or overexpression of miRNAs with potential sequence-complementarity to the ARE did not change reporter gene expression. Finally, we demonstrate that the putative precursor of Drosophila miR-289 – the miRNA that was originally found responsible for ARE recognition in Drosophila – does not give rise to a mature miRNA. We therefore conclude that in mouse embryonic fibroblasts and Drosophila S2 cells, ARE-mediated post-transcriptional control is independent of the mi/siRNA pathways. ECF-type ABC transporters are widespread among prokaryotes and involved in uptake of vitamins, transition metal cations, intermediates of salvage pathways and probably other compounds.