NDLI: Identification of a novel antisense noncoding RNA, ALID, transcribed from the putative imprinting control region of marsupial IGF2R

Content Provider	Springer Nature : BioMed Central
Author	Suzuki, Shunsuke Shaw, Geoffrey Renfree, Marilyn B.
Abstract	Background Genomic imprinting leads to maternal expression of IGF2R in both mouse and opossum. In mouse, the antisense long noncoding (lnc) RNA Airn, which is paternally expressed from the differentially methylated region (DMR) in the second intron of Igf2r, is required to silence the paternal Igf2r. In opossum, however, intriguingly, the DMR was reported to be in a different downstream intron (intron 11) and there was no antisense lncRNA detected in previous analyses. Therefore, clarifying the imprinting mechanism of marsupial IGF2R is of great relevance for understanding the origin and evolution of genomic imprinting in the IGF2R locus. Thus, the antisense lncRNA associated with the marsupial DMR can be considered as the ‘missing link’. In this study, we identified a novel antisense lncRNA, ALID, after detailed analysis of the IGF2R locus in an Australian marsupial, the tammar wallaby, Macropus eugenii, and compared it to that of the grey short-tailed opossum, Monodelphis domestica. Results Tammar IGF2R showed maternal expression and had a maternally methylated CpG island (CGI) in intron 12 as well as a promoter CGI without differential methylation, but none in the second intron. Re-analysis of the IGF2R of opossum detected the CGI in intron 12, not intron 11, as previously reported, confirming that the DMR in intron 12 is conserved between these marsupials and so is the putative imprinting control region of marsupial IGF2R. ALID is paternally expressed from the middle of the DMR and is approximately 650 bp long with a single exon structure that is extremely short compared to Airn. Hence, the lncRNA transcriptional overlap of the IGF2R promoter, which is essential for the Igf2r silencing in the mouse, is likely absent in tammar. This suggests that fundamental differences in the lncRNA-based silencing mechanisms evolved in eutherian and marsupial IGF2R and may reflect the lack of differential methylation in the promoter CGI of marsupial IGF2R. Conclusions Our study thus provides the best candidate factor for establishing paternal silencing of marsupial IGF2R without transcriptional overlap, which is distinct from the Igf2r silencing mechanism of Airn, but which may be analogous to the mode of action for the flanking Slc22a2 and Slc22a3 gene silencing in the mouse placenta.
Related Links	https://epigeneticsandchromatin.biomedcentral.com/counter/pdf/10.1186/s13072-018-0227-8.pdf
Ending Page	11
Page Count	11
Starting Page	1
File Format	HTM / HTML
ISSN	17568935
DOI	10.1186/s13072-018-0227-8
Journal	Epigenetics & Chromatin
Issue Number	1
Volume Number	11
Language	English
Publisher	BioMed Central
Publisher Date	2018-09-29
Access Restriction	Open
Subject Keyword	Animal Genetics and Genomics Human Genetics Plant Genetics and Genomics Cell Biology Gene Expression Gene Function IGF2R Genomic imprinting lncRNA Marsupials
Content Type	Text
Resource Type	Article
Subject	Genetics Molecular Biology
Journal Impact Factor	4.2/2023
5-Year Journal Impact Factor	4.9/2023

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