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
E. Dale AbelUniversity of Iowa