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Gene knockouts and murine development

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Gene knockouts and murine development. / Gatherer, Derek.
In: Development, Growth and Differentiation, Vol. 35, No. 4, 08.1993, p. 365-370.

Research output: Contribution to Journal/MagazineLiterature reviewpeer-review

Harvard

Gatherer, D 1993, 'Gene knockouts and murine development', Development, Growth and Differentiation, vol. 35, no. 4, pp. 365-370. https://doi.org/10.1111/j.1440-169X.1993.00365.x

APA

Gatherer, D. (1993). Gene knockouts and murine development. Development, Growth and Differentiation, 35(4), 365-370. https://doi.org/10.1111/j.1440-169X.1993.00365.x

Vancouver

Gatherer D. Gene knockouts and murine development. Development, Growth and Differentiation. 1993 Aug;35(4):365-370. doi: 10.1111/j.1440-169X.1993.00365.x

Author

Gatherer, Derek. / Gene knockouts and murine development. In: Development, Growth and Differentiation. 1993 ; Vol. 35, No. 4. pp. 365-370.

Bibtex

@article{dad4894beab74f47a4e60fe742409cda,
title = "Gene knockouts and murine development",
abstract = "A considerable quantity of data has been generated using the technique of in vivo gene knockout in mice, much of which is of relevance to the developmental biologist. Null mutations in Hox genes at the 3′-end of the clusters create complex irregularities at the rostral end of the embryo, including defects in the middle ear and the large blood vessels, suggesting that Hox genes may be involved in pattern specification of these structures in addition to the anteroposterior axis. Null mutations in oncogenes either cause wide pleiotropic effects, or act in a restricted manner on the haematopoietic system. Null mutations in growth factors and related molecules cause failure of proliferation in restricted areas of the embryo in some cases, but have little phenotype in others. There is as yet no null mutation which supports the idea that growth factors are involved in mesoderm induction in mammals. A surprising variety of genes have no null phenotype, or one less severe than might have been previously predicted on the basis of their known function in vitro and pattern of expression. This leads to the possibility that genetic redundancy exists in development.",
keywords = "GENE KNOCKOUT, GENE TARGETING, MUS, MAMMALIAN EMBRYOLOGY, GENETIC REDUNDANCY, TARGETED DISRUPTION, HOMEOBOX GENE, INT-1 PROTOONCOGENE, MESODERM INDUCTION, XENOPUS EMBRYOS, NULL MUTATION, C-FOS, MICE, MOUSE, EXPRESSION",
author = "Derek Gatherer",
year = "1993",
month = aug,
doi = "10.1111/j.1440-169X.1993.00365.x",
language = "English",
volume = "35",
pages = "365--370",
journal = "Development, Growth and Differentiation",
issn = "0012-1592",
publisher = "Wiley-Blackwell",
number = "4",

}

RIS

TY - JOUR

T1 - Gene knockouts and murine development

AU - Gatherer, Derek

PY - 1993/8

Y1 - 1993/8

N2 - A considerable quantity of data has been generated using the technique of in vivo gene knockout in mice, much of which is of relevance to the developmental biologist. Null mutations in Hox genes at the 3′-end of the clusters create complex irregularities at the rostral end of the embryo, including defects in the middle ear and the large blood vessels, suggesting that Hox genes may be involved in pattern specification of these structures in addition to the anteroposterior axis. Null mutations in oncogenes either cause wide pleiotropic effects, or act in a restricted manner on the haematopoietic system. Null mutations in growth factors and related molecules cause failure of proliferation in restricted areas of the embryo in some cases, but have little phenotype in others. There is as yet no null mutation which supports the idea that growth factors are involved in mesoderm induction in mammals. A surprising variety of genes have no null phenotype, or one less severe than might have been previously predicted on the basis of their known function in vitro and pattern of expression. This leads to the possibility that genetic redundancy exists in development.

AB - A considerable quantity of data has been generated using the technique of in vivo gene knockout in mice, much of which is of relevance to the developmental biologist. Null mutations in Hox genes at the 3′-end of the clusters create complex irregularities at the rostral end of the embryo, including defects in the middle ear and the large blood vessels, suggesting that Hox genes may be involved in pattern specification of these structures in addition to the anteroposterior axis. Null mutations in oncogenes either cause wide pleiotropic effects, or act in a restricted manner on the haematopoietic system. Null mutations in growth factors and related molecules cause failure of proliferation in restricted areas of the embryo in some cases, but have little phenotype in others. There is as yet no null mutation which supports the idea that growth factors are involved in mesoderm induction in mammals. A surprising variety of genes have no null phenotype, or one less severe than might have been previously predicted on the basis of their known function in vitro and pattern of expression. This leads to the possibility that genetic redundancy exists in development.

KW - GENE KNOCKOUT

KW - GENE TARGETING

KW - MUS

KW - MAMMALIAN EMBRYOLOGY

KW - GENETIC REDUNDANCY

KW - TARGETED DISRUPTION

KW - HOMEOBOX GENE

KW - INT-1 PROTOONCOGENE

KW - MESODERM INDUCTION

KW - XENOPUS EMBRYOS

KW - NULL MUTATION

KW - C-FOS

KW - MICE

KW - MOUSE

KW - EXPRESSION

U2 - 10.1111/j.1440-169X.1993.00365.x

DO - 10.1111/j.1440-169X.1993.00365.x

M3 - Literature review

VL - 35

SP - 365

EP - 370

JO - Development, Growth and Differentiation

JF - Development, Growth and Differentiation

SN - 0012-1592

IS - 4

ER -