Targeted disruption of mouse EGF receptor

Effect of genetic background on mutant phenotype

David W. Threadgill, Andrzej A. Dlugosz, Laura A. Hansen, Tamar Tennenbaum, Ulrike Lichti, Della Yee, Christian LaMantia, Tracy Mourton, Karl Herrup, Raymond C. Harris, John A. Barnard, Stuart H. Yuspa, Robert J. Coffey, Terry Magnuson

Research output: Contribution to journalArticle

1153 Citations (Scopus)

Abstract

Gene targeting was used to create a null allele at the epidermal growth factor receptor locus (Egfr). The phenotype was dependent on genetic background. EGFR deficiency on a CF-1 background resulted in peri-implantation death due to degeneration of the inner cell mass. On a 129/Sv background, homozygous mutants died at mid-gestation due to placental defects; on a CD-1 background, the mutants lived for up to 3 weeks and showed abnormalities in skin, kidney, brain, liver, and gastrointestinal tract. The multiple abnormalities associated with EGFR deficiency indicate that the receptor is involved in a wide range of cellular activities.

Original languageEnglish
Pages (from-to)230-234
Number of pages5
JournalScience
Volume269
Issue number5221
StatePublished - 1995
Externally publishedYes

Fingerprint

Skin Abnormalities
Multiple Abnormalities
Gene Targeting
Epidermal Growth Factor Receptor
Gastrointestinal Tract
Alleles
Phenotype
Kidney
Pregnancy
Liver
Brain
Genetic Background

All Science Journal Classification (ASJC) codes

  • General

Cite this

Threadgill, D. W., Dlugosz, A. A., Hansen, L. A., Tennenbaum, T., Lichti, U., Yee, D., ... Magnuson, T. (1995). Targeted disruption of mouse EGF receptor: Effect of genetic background on mutant phenotype. Science, 269(5221), 230-234.

Targeted disruption of mouse EGF receptor : Effect of genetic background on mutant phenotype. / Threadgill, David W.; Dlugosz, Andrzej A.; Hansen, Laura A.; Tennenbaum, Tamar; Lichti, Ulrike; Yee, Della; LaMantia, Christian; Mourton, Tracy; Herrup, Karl; Harris, Raymond C.; Barnard, John A.; Yuspa, Stuart H.; Coffey, Robert J.; Magnuson, Terry.

In: Science, Vol. 269, No. 5221, 1995, p. 230-234.

Research output: Contribution to journalArticle

Threadgill, DW, Dlugosz, AA, Hansen, LA, Tennenbaum, T, Lichti, U, Yee, D, LaMantia, C, Mourton, T, Herrup, K, Harris, RC, Barnard, JA, Yuspa, SH, Coffey, RJ & Magnuson, T 1995, 'Targeted disruption of mouse EGF receptor: Effect of genetic background on mutant phenotype', Science, vol. 269, no. 5221, pp. 230-234.
Threadgill DW, Dlugosz AA, Hansen LA, Tennenbaum T, Lichti U, Yee D et al. Targeted disruption of mouse EGF receptor: Effect of genetic background on mutant phenotype. Science. 1995;269(5221):230-234.
Threadgill, David W. ; Dlugosz, Andrzej A. ; Hansen, Laura A. ; Tennenbaum, Tamar ; Lichti, Ulrike ; Yee, Della ; LaMantia, Christian ; Mourton, Tracy ; Herrup, Karl ; Harris, Raymond C. ; Barnard, John A. ; Yuspa, Stuart H. ; Coffey, Robert J. ; Magnuson, Terry. / Targeted disruption of mouse EGF receptor : Effect of genetic background on mutant phenotype. In: Science. 1995 ; Vol. 269, No. 5221. pp. 230-234.
@article{36424ab759234e0fb4378474c17d1b9a,
title = "Targeted disruption of mouse EGF receptor: Effect of genetic background on mutant phenotype",
abstract = "Gene targeting was used to create a null allele at the epidermal growth factor receptor locus (Egfr). The phenotype was dependent on genetic background. EGFR deficiency on a CF-1 background resulted in peri-implantation death due to degeneration of the inner cell mass. On a 129/Sv background, homozygous mutants died at mid-gestation due to placental defects; on a CD-1 background, the mutants lived for up to 3 weeks and showed abnormalities in skin, kidney, brain, liver, and gastrointestinal tract. The multiple abnormalities associated with EGFR deficiency indicate that the receptor is involved in a wide range of cellular activities.",
author = "Threadgill, {David W.} and Dlugosz, {Andrzej A.} and Hansen, {Laura A.} and Tamar Tennenbaum and Ulrike Lichti and Della Yee and Christian LaMantia and Tracy Mourton and Karl Herrup and Harris, {Raymond C.} and Barnard, {John A.} and Yuspa, {Stuart H.} and Coffey, {Robert J.} and Terry Magnuson",
year = "1995",
language = "English",
volume = "269",
pages = "230--234",
journal = "Science",
issn = "0036-8075",
publisher = "American Association for the Advancement of Science",
number = "5221",

}

TY - JOUR

T1 - Targeted disruption of mouse EGF receptor

T2 - Effect of genetic background on mutant phenotype

AU - Threadgill, David W.

AU - Dlugosz, Andrzej A.

AU - Hansen, Laura A.

AU - Tennenbaum, Tamar

AU - Lichti, Ulrike

AU - Yee, Della

AU - LaMantia, Christian

AU - Mourton, Tracy

AU - Herrup, Karl

AU - Harris, Raymond C.

AU - Barnard, John A.

AU - Yuspa, Stuart H.

AU - Coffey, Robert J.

AU - Magnuson, Terry

PY - 1995

Y1 - 1995

N2 - Gene targeting was used to create a null allele at the epidermal growth factor receptor locus (Egfr). The phenotype was dependent on genetic background. EGFR deficiency on a CF-1 background resulted in peri-implantation death due to degeneration of the inner cell mass. On a 129/Sv background, homozygous mutants died at mid-gestation due to placental defects; on a CD-1 background, the mutants lived for up to 3 weeks and showed abnormalities in skin, kidney, brain, liver, and gastrointestinal tract. The multiple abnormalities associated with EGFR deficiency indicate that the receptor is involved in a wide range of cellular activities.

AB - Gene targeting was used to create a null allele at the epidermal growth factor receptor locus (Egfr). The phenotype was dependent on genetic background. EGFR deficiency on a CF-1 background resulted in peri-implantation death due to degeneration of the inner cell mass. On a 129/Sv background, homozygous mutants died at mid-gestation due to placental defects; on a CD-1 background, the mutants lived for up to 3 weeks and showed abnormalities in skin, kidney, brain, liver, and gastrointestinal tract. The multiple abnormalities associated with EGFR deficiency indicate that the receptor is involved in a wide range of cellular activities.

UR - http://www.scopus.com/inward/record.url?scp=0029064203&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0029064203&partnerID=8YFLogxK

M3 - Article

VL - 269

SP - 230

EP - 234

JO - Science

JF - Science

SN - 0036-8075

IS - 5221

ER -