ArticleActa physiologica (Oxford, England)2014
Perturbations to the IGF1 growth pathway and adult energy homeostasis following disruption of mouse chromosome 12 imprinting.
Article in Acta physiologica (Oxford, England), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 13 citations in OpenAlex.
- Transgenerational epigenetic self-memory ofEpigenetics · 2024Article
- The imprintedeLife · 2022Article
- Paternally expressed gene 3 (Pw1/Peg3) promotes sexual dimorphism in metabolism and behavior.PLoS genetics · 2022Article
- Temple syndrome and Kagami-Ogata syndrome: clinical presentations, genotypes, models and mechanisms.Human molecular genetics · 2020Review
- Silencing of retrotransposon-derived imprinted gene RTL1 is the main cause for postimplantational failures in mammalian cloning.Proceedings of the National Academy of Sciences of the United States of America · 2018Article
- The Type 3 Deiodinase: Epigenetic Control of Brain Thyroid Hormone Action and Neurological Function.International journal of molecular sciences · 2018Review
- From Pre-Clinical Studies to Clinical Trials: Generation of Novel Therapies for Pregnancy Complications.International journal of molecular sciences · 2015Review
- Insulin and insulin-like growth factor 1 receptors are required for normal expression of imprinted genes.Proceedings of the National Academy of Sciences of the United States of America · 2014Article
- The miR-379/miR-410 cluster at the imprinted Dlk1-Dio3 domain controls neonatal metabolic adaptation.The EMBO journal · 2014Article
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Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
Abstract
aimDisruption to insulin-like growth factor (IGF) signalling pathways during early life causes growth retardation and defects of developing metabolic organs that can alter set points of energy homeostasis for a lifetime. Inheritance of two maternal copies of human chromosome 14q32.2 (Temple syndrome) causes severe foetal growth retardation and post-natal failure to thrive. Disruption of imprinted gene dosage in the orthologous region on mouse chromosome 12 also affects growth. Here, we investigated whether altering chromosome 12-imprinted gene dosage can affect IGF signalling.
methodsWe investigated mice with a transgene insertion at the imprinted domain of chromosome 12. This lesion causes misexpression of neighbouring genes such that the expression of non-coding RNAs is elevated, and levels of delta-like homologue 1 (Dlk1), retrotransposon-like 1 (Rtl1) and deiodinase 3 (Dio3) transcripts are reduced.
resultsWe observed three key phenotypes in these mice: (i) embryonic growth retardation associated with altered expression of IGF1 binding proteins, (ii) peri-natal failure to thrive accompanied by hypothyroidism and low serum IGF1. Unexpectedly this phenotype was growth hormone independent. (iii) Adult animals had reduced glucose tolerance as a result of endocrine pancreatic insufficiency.
conclusionsWe propose that all of these phenotypes are attributable to impaired IGF action and show for the first time that the chromosome 12 cluster in the mouse is an imprinted locus that modulates the IGF signalling pathway. We propose that growth retardation observed in human Temple syndrome might have a similar cause.
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