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Cell depletion due to diphtheria toxin fragment A after Cre-mediated recombination

Cell depletion due to diphtheria toxin fragment A after Cre-mediated recombination
Cell depletion due to diphtheria toxin fragment A after Cre-mediated recombination
Abnormal cell loss is the common cause of a large number of developmental and degenerative diseases. To model such diseases in transgenic animals, we have developed a line of mice that allows the efficient depletion of virtually any cell type in vivo following somatic Cre-mediated gene recombination. By introducing the diphtheria toxin fragment A (DT-A) gene as a conditional expression construct (floxed lacZ-DT-A) into the ubiquitously expressed ROSA26 locus, we produced a line of mice that would permit cell-specific activation of the toxin gene. Following Cre-mediated recombination under the control of cell-type-specific promoters, lacZ gene expression was efficiently replaced by de novo transcription of the Cre-recombined DT-A gene. We provide proof of this principle, initially for cells of the central nervous system (pyramidal neurons and oligodendrocytes), the immune system (B cells), and liver tissue (hepatocytes), that the conditional expression of DT-A is functional in vivo, resulting in the generation of novel degenerative disease models.
0270-7306
7636-7642
Brockschnieder, D.
766bdfda-70f4-4c9d-82e4-96ab38497161
Lappe-Siefke, C.
69acb4a7-ce08-4e0b-b798-15f534df71c7
Goebbels, S.
00dc65ab-1a0b-4fa2-8603-2f1e88b60382
Boesl, M.R.
935fdd19-e4b8-49f9-9fda-004ecc44a57c
Nave, K.A.
f9379901-93f2-4576-b842-58bfa5b285b9
Riethmacher, D.
1a0a0c2e-e94d-4d0a-a890-90107a2545bc
Brockschnieder, D.
766bdfda-70f4-4c9d-82e4-96ab38497161
Lappe-Siefke, C.
69acb4a7-ce08-4e0b-b798-15f534df71c7
Goebbels, S.
00dc65ab-1a0b-4fa2-8603-2f1e88b60382
Boesl, M.R.
935fdd19-e4b8-49f9-9fda-004ecc44a57c
Nave, K.A.
f9379901-93f2-4576-b842-58bfa5b285b9
Riethmacher, D.
1a0a0c2e-e94d-4d0a-a890-90107a2545bc

Brockschnieder, D., Lappe-Siefke, C., Goebbels, S., Boesl, M.R., Nave, K.A. and Riethmacher, D. (2004) Cell depletion due to diphtheria toxin fragment A after Cre-mediated recombination. Molecular and Cellular Biology, 24 (17), 7636-7642. (doi:10.1128/MCB.24.17.7636-7642.2004).

Record type: Article

Abstract

Abnormal cell loss is the common cause of a large number of developmental and degenerative diseases. To model such diseases in transgenic animals, we have developed a line of mice that allows the efficient depletion of virtually any cell type in vivo following somatic Cre-mediated gene recombination. By introducing the diphtheria toxin fragment A (DT-A) gene as a conditional expression construct (floxed lacZ-DT-A) into the ubiquitously expressed ROSA26 locus, we produced a line of mice that would permit cell-specific activation of the toxin gene. Following Cre-mediated recombination under the control of cell-type-specific promoters, lacZ gene expression was efficiently replaced by de novo transcription of the Cre-recombined DT-A gene. We provide proof of this principle, initially for cells of the central nervous system (pyramidal neurons and oligodendrocytes), the immune system (B cells), and liver tissue (hepatocytes), that the conditional expression of DT-A is functional in vivo, resulting in the generation of novel degenerative disease models.

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Published date: September 2004

Identifiers

Local EPrints ID: 48498
URI: http://eprints.soton.ac.uk/id/eprint/48498
ISSN: 0270-7306
PURE UUID: 57437159-e6dc-47ce-860e-63efa3e50ff7
ORCID for D. Riethmacher: ORCID iD orcid.org/0000-0002-4206-5529

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Date deposited: 26 Sep 2007
Last modified: 08 Oct 2019 00:43

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Contributors

Author: D. Brockschnieder
Author: C. Lappe-Siefke
Author: S. Goebbels
Author: M.R. Boesl
Author: K.A. Nave
Author: D. Riethmacher ORCID iD

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