Rheb is essential for murine development

Susanna M.I. Goorden; Marianne Hoogeveen-Westerveld; Caroline Cheng; Geeske M. van Woerden; Melika Mozaffari; Laura Post; Henricus J. Duckers; Mark Nellist; Ype Elgersma

doi:10.1128/MCB.00985-10

Rheb is essential for murine development

Susanna M.I. Goorden
, Marianne Hoogeveen-Westerveld
, Caroline Cheng
, Geeske M. van Woerden
, Melika Mozaffari
, Laura Post
, Henricus J. Duckers
, Mark Nellist
, Ype Elgersma^*

^*Corresponding author for this work

Research output: Contribution to journal › Article › Academic › peer-review

Abstract

Ras homolog enriched in brain (Rheb) couples growth factor signaling to activation of the target of rapamycin complex 1 (TORC1). To study its role in mammals, we generated a Rheb knockout mouse. In contrast to mTOR or regulatory-associated protein of mTOR (Raptor) mutants, the inner cell mass of Rheb^-/- embryos differentiated normally. Nevertheless, Rheb^-/- embryos died around midgestation, most likely due to impaired development of the cardiovascular system. Rheb^-/- embryonic fibroblasts showed decreased TORC1 activity, were smaller, and showed impaired proliferation. Rheb heterozygosity extended the life span of tuberous sclerosis complex 1-deficient (Tsc1^-/-) embryos, indicating that there is a genetic interaction between the Tsc1 and Rheb genes in mouse.

Original language	English
Pages (from-to)	1672-1678
Number of pages	7
Journal	Molecular and Cellular Biology
Volume	31
Issue number	8
DOIs	https://doi.org/10.1128/MCB.00985-10
Publication status	Published - Apr 2011
Externally published	Yes

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title = "Rheb is essential for murine development",

abstract = "Ras homolog enriched in brain (Rheb) couples growth factor signaling to activation of the target of rapamycin complex 1 (TORC1). To study its role in mammals, we generated a Rheb knockout mouse. In contrast to mTOR or regulatory-associated protein of mTOR (Raptor) mutants, the inner cell mass of Rheb-/- embryos differentiated normally. Nevertheless, Rheb-/- embryos died around midgestation, most likely due to impaired development of the cardiovascular system. Rheb-/- embryonic fibroblasts showed decreased TORC1 activity, were smaller, and showed impaired proliferation. Rheb heterozygosity extended the life span of tuberous sclerosis complex 1-deficient (Tsc1-/-) embryos, indicating that there is a genetic interaction between the Tsc1 and Rheb genes in mouse.",

author = "Goorden, \{Susanna M.I.\} and Marianne Hoogeveen-Westerveld and Caroline Cheng and \{van Woerden\}, \{Geeske M.\} and Melika Mozaffari and Laura Post and Duckers, \{Henricus J.\} and Mark Nellist and Ype Elgersma",

year = "2011",

month = apr,

doi = "10.1128/MCB.00985-10",

language = "English",

volume = "31",

pages = "1672--1678",

journal = "Molecular and Cellular Biology",

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TY - JOUR

T1 - Rheb is essential for murine development

AU - Goorden, Susanna M.I.

AU - Hoogeveen-Westerveld, Marianne

AU - Cheng, Caroline

AU - van Woerden, Geeske M.

AU - Mozaffari, Melika

AU - Post, Laura

AU - Duckers, Henricus J.

AU - Nellist, Mark

AU - Elgersma, Ype

PY - 2011/4

Y1 - 2011/4

N2 - Ras homolog enriched in brain (Rheb) couples growth factor signaling to activation of the target of rapamycin complex 1 (TORC1). To study its role in mammals, we generated a Rheb knockout mouse. In contrast to mTOR or regulatory-associated protein of mTOR (Raptor) mutants, the inner cell mass of Rheb-/- embryos differentiated normally. Nevertheless, Rheb-/- embryos died around midgestation, most likely due to impaired development of the cardiovascular system. Rheb-/- embryonic fibroblasts showed decreased TORC1 activity, were smaller, and showed impaired proliferation. Rheb heterozygosity extended the life span of tuberous sclerosis complex 1-deficient (Tsc1-/-) embryos, indicating that there is a genetic interaction between the Tsc1 and Rheb genes in mouse.

AB - Ras homolog enriched in brain (Rheb) couples growth factor signaling to activation of the target of rapamycin complex 1 (TORC1). To study its role in mammals, we generated a Rheb knockout mouse. In contrast to mTOR or regulatory-associated protein of mTOR (Raptor) mutants, the inner cell mass of Rheb-/- embryos differentiated normally. Nevertheless, Rheb-/- embryos died around midgestation, most likely due to impaired development of the cardiovascular system. Rheb-/- embryonic fibroblasts showed decreased TORC1 activity, were smaller, and showed impaired proliferation. Rheb heterozygosity extended the life span of tuberous sclerosis complex 1-deficient (Tsc1-/-) embryos, indicating that there is a genetic interaction between the Tsc1 and Rheb genes in mouse.

UR - https://www.scopus.com/pages/publications/79953140523

U2 - 10.1128/MCB.00985-10

DO - 10.1128/MCB.00985-10

M3 - Article

C2 - 21321084

AN - SCOPUS:79953140523

SN - 0270-7306

VL - 31

SP - 1672

EP - 1678

JO - Molecular and Cellular Biology

JF - Molecular and Cellular Biology

IS - 8

ER -

Rheb is essential for murine development

Abstract

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