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Publications
Publication
Mechanistic target of rapamycin (Mtor) is essential for murine embryonic heart
development and growth.
Authors
Zhu Y, Pires KM, Whitehead KJ, Olsen CD, Wayment B, Zhang YC, Bugger H, Ilkun O,
Litwin SE, Thomas G, Kozma SC, Abel ED
Submitted By
E. Dale Abel on 3/4/2015
Status
Published
Journal
PLoS ONE
Year
2013
Date Published
Volume : Pages
8 : e54221
PubMed Reference
23342106
Abstract
Mechanistic target of rapamycin (Mtor) is required for embryonic inner cell mass
proliferation during early development. However, Mtor expression levels are very
low in the mouse heart during embryogenesis. To determine if Mtor plays a role
during mouse cardiac development, cardiomyocyte specific Mtor deletion was
achieved using a myosin heavy chain (a-MHC) driven Cre recombinase. Initial
mosaic expression of Cre between embryonic day (E) 10.5 and E11.5 eliminated a
subset of cardiomyocytes with high Cre activity by apoptosis and reduced overall
cardiac proliferative capacity. The remaining cardiomyocytes proliferated and
expanded normally. However loss of 50% of cardiomyocytes defined a threshold
that impairs the ability of the embryonic heart to sustain the embryo's
circulatory requirements. As a result 92% of embryos with cardiomyocyte Mtor
deficiency died by the end of gestation. Thus Mtor is required for survival and
proliferation of cardiomyocytes in the developing heart.
Investigators with authorship
Name
Institution
E. Dale Abel
University of Iowa
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Please acknowledge all posters, manuscripts or scientific materials that were generated in part or whole using funds from the Diabetic Complications Consortium(DiaComp) using the following text:
Financial support for this work provided by the NIDDK Diabetic Complications Consortium (RRID:SCR_001415, www.diacomp.org), grants DK076169 and DK115255
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