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

doi:10.1126/science.7618084

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

Department of Biomedical Sciences

Research output: Contribution to journal › Article

1177 Scopus citations

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 language	English (US)
Pages (from-to)	230-234
Number of pages	5
Journal	Science
Volume	269
Issue number	5221
DOIs	https://doi.org/10.1126/science.7618084
State	Published - Jan 1 1995

Fingerprint

All Science Journal Classification (ASJC) codes

General

Cite this

Threadgill, D. W., Dlugosz, A. A., Hansen, L. A., Tennenbaum, T., Lichti, U., Yee, D., LaMantia, C., Mourton, T., Herrup, K., Harris, R. C., Barnard, J. A., Yuspa, S. H., Coffey, R. J., & Magnuson, T. (1995). Targeted disruption of mouse EGF receptor: Effect of genetic background on mutant phenotype. Science, 269(5221), 230-234. https://doi.org/10.1126/science.7618084

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, 01.01.1995, p. 230-234.

Research output: Contribution to journal › Article

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",

month = jan

day = "1",

doi = "10.1126/science.7618084",

language = "English (US)",

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 - 1995/1/1

Y1 - 1995/1/1

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

U2 - 10.1126/science.7618084

DO - 10.1126/science.7618084

M3 - Article

C2 - 7618084

AN - SCOPUS:0029064203

VL - 269

SP - 230

EP - 234

JO - Science

JF - Science

SN - 0036-8075

IS - 5221

ER -

Access to Document

10.1126/science.7618084