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Many mammalian genes contain overlapping antisense RNAs, but the functions and mechanisms of action of these transcripts are mostly unknown.  WT1  is a well-characterized developmental gene that is mutated in Wilms’ tumor (WT) and acute myeloid leukaemia (AML) and has an antisense transcript ( WT1-AS ), which we have previously found to regulate WT1 protein levels. In this study, we show that  WT1-AS  is present in multiple spliceoforms that are usually expressed in parallel with  WT1  RNA in human and mouse tissues. We demonstrate that the expression of  WT1-AS  correlates with methylation of the antisense regulatory region (ARR) in  WT1  intron 1, displaying imprinted monoallelic expression in normal kidney and loss of imprinting in WT. However, we find no evidence for imprinting of mouse  Wt1-as. WT1-AS  transcripts are exported into the cytoplasm and form heteroduplexes with  WT1  mRNA in the overlapping region in  WT1  exon 1. In AML, there is often abnormal splicing of  WT1-AS , which may play a role in the development of this malignancy. These results show that  WT1  encodes conserved antisense RNAs that may have an important regulatory role in WT1 expression via RNA:RNA interactions, and which can become deregulated by a variety of mechanisms in cancer.

Alternately spliced WT1 antisense transcripts interact with WT1 sense RNA and show epigenetic and splicing defects in cancer