ArticleBMC developmental biology2010
Rescue of placental phenotype in a mechanistic model of Beckwith-Wiedemann syndrome.
Article in BMC developmental biology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 11 citations in OpenAlex.
- Article
- Fetal growth restriction in a genetic model of sporadic Beckwith-Wiedemann syndrome.Disease models & mechanisms · 2018Article
- Transcription factor ASCL2 is required for development of the glycogen trophoblast cell lineage.PLoS genetics · 2018Article
- Predicted protein interactions of IFITMs may shed light on mechanisms of Zika virus-induced microcephaly and host invasion.F1000Research · 2016Article
- The placental imprintome and imprinted gene function in the trophoblast glycogen cell lineage.Reproductive biomedicine online · 2012Review
- Partial loss of Ascl2 function affects all three layers of the mature placenta and causes intrauterine growth restriction.Developmental biology · 2011Article
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Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
Abstract
backgroundSeveral imprinted genes have been implicated in the process of placentation. The distal region of mouse chromosome 7 (Chr 7) contains at least ten imprinted genes, several of which are expressed from the maternal homologue in the placenta. The corresponding paternal alleles of these genes are silenced in cis by an incompletely understood mechanism involving the formation of a repressive nuclear compartment mediated by the long non-coding RNA Kcnq1ot1 initiated from imprinting centre 2 (IC2). However, it is unknown whether some maternally expressed genes are silenced on the paternal homologue via a Kcnq1ot1-independent mechanism. We have previously reported that maternal inheritance of a large truncation of Chr7 encompassing the entire IC2-regulated domain (DelTel7 allele) leads to embryonic lethality at mid-gestation accompanied by severe placental abnormalities. Kcnq1ot1 expression can be abolished on the paternal chromosome by deleting IC2 (IC2KO allele). When the IC2KO mutation is paternally inherited, epigenetic silencing is lost in the region and the DelTel7 lethality is rescued in compound heterozygotes, leading to viable DelTel7/IC2KO mice.
resultsConsidering the important functions of several IC2-regulated genes in placentation, we set out to determine whether these DelTel7/IC2KO rescued conceptuses develop normal placentae. We report no abnormalities with respect to the architecture and vasculature of the DelTel7/IC2KO rescued placentae. Imprinted expression of several of the IC2-regulated genes critical to placentation is also faithfully recapitulated in DelTel7/IC2KO placentae.
conclusionTaken together, our results demonstrate that all the distal chromosome 7 imprinted genes implicated in placental function are silenced by IC2 and Kcnq1ot1 on the paternal allele. Furthermore, our results demonstrate that the methylated maternal IC2 is not required for the regulation of nearby genes. The results show the potential for fully rescuing LQ trans placental abnormalities that are caused by imprinting defects.
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