Research
Imprinting is a phenomenon whereby certain genes are expressed preferentially from one allele in a parent-of-origin specific manner and is essential for mammalian development. Most genes subject to imprinting are associated with differentially DNA methylated regions established by, or dependent on, de novo DNA methylation in gametes. However conceptuses derived from oocytes with specific knock-outs of de novo DNA methyltransferases have no loss of imprinting for a subset of genes in trophoblast lineages, termed non-canonically imprinted (NCI). NCI genes are all associated with nearby LTR elements, with the majority also subject to placental specific imprinting. Initial analysis of publically available datasets reveals that cultured hybrid mouse trophoblast stem cells (TSCs) recapitulate the imprinted expression of NCI genes. Future work will focus on the characterisation of NCI LTR knock-outs in TSCs to establish whether LTRs are required for NCI expression and determine the function of this expression in development.
Publications
Maternal H3K27me3 controls DNA methylation-independent imprinting. Inoue et al. Nature (2017) (First paper to characterise the role of maternal chromatin in DNA-methylation independent imprinting).
Endogenous retroviral insertions drive non-canonical imprinting in extra-embryonic tissues. Hanna et al. Genome Biol. (2019) (The Kelsey lab paper that led to my current research topic, revealing non-canonical imprinting specifically in the trophoblast derived lineages of the conceptus).
Evolution of imprinting via lineage-specific insertion of retroviral promoters Bogutz et al. Nat. Comms. (2019) (this paper reveals the role of ERV elements promoting oocyte transcription to drive canonical imprinting through stimulation of maternal allele DNA methylation).
