MCB Accepts, published online ahead of print on 2 November 2009

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Mol. Cell. Biol. doi:10.1128/MCB.00662-09
Copyright (c) 2009, American Society for Microbiology and/or the Listed Authors/Institutions. All Rights Reserved.

The imprinted Phlda2 gene regulates extraembryonic energy stores.

S. J. Tunster, B Tycko, and R. M. John^*

Genetics Division, Cardiff School of Biosciences, Cardiff University, Cardiff, Wales, CF10 3US, UK; Institute for Cancer Genetics and Department of Pathology, Columbia University College of Physicians and Surgeons, 1130 St Nicholas Avenue, New York, New York 10032, USA

^* To whom correspondence should be addressed. Email: JohnRM{at}cf.ac.uk.

An important difference between placental mammals and marsupials is the maturity of the fetus at birth. Placental mammals achieved this maturity by developing a complex and invasive placenta to support and prolong internal development. The exact genomic modifications that facilitated the evolution of this complex structure are unknown but the emergence of genomic imprinting within mammalian lineages suggests a role for gene dosage. Here we show that a maximally altered placental structure is achieved by a single extra dose of the imprinted Phlda2 gene characterised by a dramatically reduced junctional zone and a decrease in stored glycogen. In addition, glycogen cells do not migrate into the maternal decidua in a timely fashion but instead Tpbpa positive cells progressively mislocalise into the labyrinthe. These defects are linked to a progressive restriction of embryonic growth from E16.5. This work has identified a critical role for the imprinted Phlda2 gene in regulating glycogen storage in the eutherian placenta and implies that imprinting has provided a mechanism to boost nutrient supply to the fetus late in gestation, when the fetus is placing the highest demands on maternal resources, to enhance growth.