Insulin-like growth factor antisense gene (Igf2as) expression was investigated in different mouse tissues during development, in differentiating C2C12 cells and in a DMR1-U2 knockout mouse model. The expression levels of Igf2as were high in fetal and newborn liver and muscle tissues compared to adults. The Igf2as gene was also expressed in placenta and in brain. The expression data suggests that the Igf2as gene plays a role in early development of the mouse and in placenta. There was no consistent evidence for an interaction between Igf2 and Igf2as transcripts. Furthermore, in knockout placentas lacking Igf2as transcription, Igf2 expression was comparable to that in wild type. These results indicate that Igf2as does not regulate Igf2 sense transcripts. In previous studies, it was suggested that the DMR1-U2 knockout mouse showing intrauterine growth restriction was caused by the absence of placenta-specific Igf2 P0 transcription. We conclude that the DMR1-U2 deletion phenotype should be reconsidered in the light of a functional Igf2as gene. 1. Introduction The insulin-like growth factor 2 gene (Igf2) is an imprinted gene, paternally expressed and encodes for the insulin-like growth factor II peptide [1, 2]. In mice the Igf2 gene has five promoters, from which three main transcripts, a placenta specific transcript and a newly described mesoderm-specific transcript, originate [3]. Moore et al. [4] described multiple imprinted sense and antisense transcripts from the Igf2 locus. The Igf2as gene located within Igf2 is transcribed from the complementary DNA strand. We recently found that Igf2as transcripts are located in the cytoplasm and associated with polysomes indicating a protein coding function [5]. To further elucidate the function of Igf2as, we investigated the DMR1-U2 knockout mouse [6]. This mouse has a 5？kb deletion within the Igf2 gene comprising DMR1, an adjacent repeat sequence mostly embedded in exon U2 of the placenta specific Igf2 P0 transcript and Igf2as transcripts. The maternal transmission of the DMR1-U2 deletion results in loss of Igf2 imprinting in heart, kidney, and lung without affecting H19 gene expression [6]. The authors conclude that their result demonstrates that DMR1 plays a role in Igf2 imprinting regulation and gene expression independent of H19 [6]. In that study, paternal transmission of the DMR1-U2 deletion was associated with intrauterine growth restriction (IUGR) manifested by mutants birth weight being 71% that of normal mice. Later, Constancia et al. [7] reported that the 5？kb DMR1-U2 deletion abolishes expression of
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