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Mechanistic Target of Rapamycin (Mtor) Is Essential for Murine Embryonic Heart Development and Growth

by Ilkun, Olesya , Whitehead, Kevin J. , Zhang, Yi Cheng , Abel, E. Dale , Zhu, Yi , Wayment, Benjamin , Litwin, Sheldon E. , Thomas, George , Pires, Karla M. P. , Olsen, Curtis D. , Bugger, Heiko , Kozma, Sara C.

in Adipocytes / Animals / Apoptosis / Biochemistry / Biology / Blotting, Western / Cardiology / Cardiomyocytes / Clonal deletion / Cre recombinase / Developmental biology / Diabetes / Embryogenesis / Embryonic development / Embryonic Development - genetics / Embryonic Development - physiology / Embryonic growth stage / Embryos / Endocrinology / Female / Gene expression / Gestation / Heart / Heart - embryology / Heart diseases / Heart failure / Hematology / Internal medicine / Kinases / Laboratory animals / Medicine / Metabolic disorders / Mice / Mice, Knockout / Muscle proteins / Musculoskeletal system / Myosin / Phosphorylation / Proteins / Rapamycin / Recombinase / Rodents / Salt / Stem cells / TOR protein / TOR Serine-Threonine Kinases - genetics / TOR Serine-Threonine Kinases - metabolism

2013

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Mechanistic Target of Rapamycin (Mtor) Is Essential for Murine Embryonic Heart Development and Growth

2013

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Mechanistic Target of Rapamycin (Mtor) Is Essential for Murine Embryonic Heart Development and Growth

2013

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Journal Article

Mechanistic Target of Rapamycin (Mtor) Is Essential for Murine Embryonic Heart Development and Growth

Ilkun, Olesya,

Whitehead, Kevin J.,

Zhang, Yi Cheng,

Abel, E. Dale,

Zhu, Yi,

Wayment, Benjamin,

Litwin, Sheldon E.,

Thomas, George,

Pires, Karla M. P.,

Olsen, Curtis D.,

Bugger, Heiko,

Kozma, Sara C.

2013

Overview

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 α myosin heavy chain (α-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.

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Publisher

Public Library of Science,Public Library of Science (PLoS)

Subject

/ Animals

/ Biology