ArticleProceedings of the National Academy of Sciences of the United States of America2002
Placental overgrowth in mice lacking the imprinted gene Ipl.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 81 papers, 1 of them a synthesis that pooled it.
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Who cites it
81 citing papers in PubMed, 1 synthesis or guideline pooled it, 216 citations in OpenAlex.
- A systematic review on the role of paternal factors in human placental development, function, and pregnancy-related disorders.Journal of assisted reproduction and genetics · 2025Pooled it
- Generation of human-induced pluripotent stem cells from a patient with Beckwith-Wiedemann syndrome.Human cell · 2025Article
- PHLDA2-mediated phosphatidic acid peroxidation triggers a distinct ferroptotic response during tumor suppression.Cell metabolism · 2024Article
- Fetal growth at term and placental oxidative stress in a tissue micro-array model: a histological and immunohistochemistry study.Histochemistry and cell biology · 2023Article
- Characterizing the role of Phlda3 in the development of acute toxicity and malignant transformation of hematopoietic cells induced by total-body irradiation in mice.Scientific reports · 2023Article
- Diagnostic Utility of TSSC3 and RB1 Immunohistochemistry in Hydatidiform Mole.International journal of molecular sciences · 2023Article
- Paternal age impairs in vitro embryo and in vivo fetal development in murine.Scientific reports · 2022Article
- In support of the placental programming hypothesis: Placental endocrine insufficiency programs atypical behaviour in mothers and their offspring.Experimental physiology · 2022Review
- The X-linked splicing regulator MBNL3 has been co-opted to restrict placental growth in eutherians.PLoS biology · 2022Article
- Epigenetic processes during preeclampsia and effects on fetal development and chronic health.Clinical science (London, England : 1979) · 2021Review
- Placental endocrine insufficiency programs anxiety, deficits in cognition and atypical social behaviour in offspring.Human molecular genetics · 2021Article
- Deletion of the ImprintedGenes · 2021Article
- Modeling human epigenetic disorders in mice: Beckwith-Wiedemann syndrome and Silver-Russell syndrome.Disease models & mechanisms · 2020Review
- Genomic imprinting and its effects on postnatal growth and adult metabolism.Cellular and molecular life sciences : CMLS · 2019Review
- Extraembryonic heparin-binding epidermal growth factor-like growth factor deficiency compromises placentation in mice.Biology of reproduction · 2019Article
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- Fetal growth restriction in a genetic model of sporadic Beckwith-Wiedemann syndrome.Disease models & mechanisms · 2018Article
- PHLDA1, another PHLDA family protein that inhibits Akt.Cancer science · 2018Article
- Maternal care boosted by paternal imprinting in mammals.PLoS biology · 2018Article
21 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The Ipl (Tssc3) gene lies in an extended imprinted region of distal mouse chromosome 7, which also contains the Igf2 gene. Expression of Ipl is highest in placenta and yolk sac, where its mRNA is derived almost entirely from the maternal allele. Ipl encodes a small cytoplasmic protein with a pleckstrin-homology (PH) domain. We constructed two lines of mice with germ-line deletions of this gene (Ipl(neo) and Ipl(loxP)) and another line deleted for the similar but nonimprinted gene Tih1. All three lines were viable. There was consistent overgrowth of the Ipl-null placentas, with expansion of the spongiotrophoblast. These larger placentas did not confer a fetal growth advantage; fetal size was normal in Ipl nulls with the Ipl(neo) allele and was decreased slightly in nulls with the Ipl(loxP) allele. When bred into an Igf2 mutant background, the Ipl deletion partially rescued the placental but not fetal growth deficiency. Neither fetal nor placental growth was affected by deletion of Tih1. These results show a nonredundant function for Ipl in restraining placental growth. The data further indicate that Ipl can act, at least in part, independently of insulin-like growth factor-2 signaling. Thus, genomic imprinting regulates multiple pathways to control placental size.
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