Nat. Genet. 35, 215–217 (2003)

Figure 1a incorrectly showed that the disruption targeted the first RNase III domain. This error also occurred throughout the text. In fact, the construct targets the second RNase III domain, which contains both canonical and noncanonical active sites. Because both RNase III domains are thought to pair intramolecularly to form an active Dicer, the construct that targets the second RNase III domain is also predicted to be a null allele. This is confirmed by the mutant shown in Figure 1d, in which sequences removed from human Dicer indeed corresponded to those removed from the mouse (correctly listed as residues 1,686–1,728 but incorrectly attributed to the first RNase III domain). Finally, since the targeting construct was generated, ENSEMBL has updated the mouse Dicer1 gene prediction, renumbering the exons. In the current release, the exon targeted in our disruption is exon 23. We apologize for this error but note that it does not alter the data presented, its interpretations or the conclusions of the paper. Corrected versions of Figure 1a and b appear below.

Figure 1: Disruption of the mouse gene Dicer1.
figure 1

(a) The targeting strategy for the Dicer1 disruption replaces the first RNase III domain with a PGK-neor expression cassette. This domain is encoded in exon 21. (b) Details of the targeting strategy. Red diamonds indicate the limits of the homology region in the targeting vector. ES cell lines containing homologous recombinants (designated by arrows) were identified by Southern blotting (c) with a probe derived from regions outside the targeting vector (indicated in b). Dicer activity of a mutated DICER1 cDNA comprising essentially the deletion introduced into the mouse gene was tested using immunoaffinity-purified protein (d). Comparison of wild-type (Dicer) and mutant (Dicer ΔRIII) proteins shows lack of siRNA production by the mutant. For comparison, processing reactions lacking extract and in Drosophila S2 cell extracts are shown.

Full size image