129S-Parp1^tm1Zqw/J

Stock number: 002779
Product name: ADPRT^-
Research areas: Apoptosis Research, Cancer Research, Immunology, Inflammation and Autoimmunity Research, Neurobiology Research

Description

Poly(ADP-ribose) polymerase-1 knock-out mice may be useful in studying DNA repair, programmed cell death, aging, differentiation, proliferation and tumor transformation.

Detailed description

Mice that are homozygous for the poly(ADP-ribose) polymerase-1 null mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. Although a shortened transcript is generated, no enzymatic activity is detected in tissues. Proliferation of homozygous fibroblasts and thymocytes is impaired following gamma-radiation in comparison to cells derived from wildtype mice. Older mice are susceptible to spontaneous development of skin disease. A significant portion of older mice (~30%) can be expected to exhibit epidermal hyperplasia. Null mice are also less susceptible to damage induced by the neurotoxin MPTP.

Development

A targeting vector containing a neomycin resistance gene was used to disrupt exon 2. The construct was electroporated into 129S2/SvPas-derived D3 embryonic stem (ES) cells. Correctly targeted ES cells were injected into C57BL/6 blastocysts. Chimeric animals were obtained and bred to 129S6/SvEv mice. This strain originated and is maintained on a 129S background.

Allele

Symbol: Parp1^tm1Zqw
Name: targeted mutation 1, Zhao-Qi Wang
MGI accession ID: MGI:1857862
Generation method: Targeted
Attributes: Null/Knockout
Synonyms: ADPRT^-; Adprt1^tm1Wag; ARTD1^-; PARP-; PARP-1-; PARS^-; PKO
Marker symbol: Parp1
Marker name: poly (ADP-ribose) polymerase family, member 1
Marker synonyms: 5830444G22Rik; Adprp; ADPRT; ADPRT 1; Adprt1; ARTD1; pADPRT-1; PARP; PARP-1; PARS; Poly-PARP; PPOL; sPARP-1
Chromosome: 1
Strain of origin: 129S2/SvPas
Molecular note: A promoterless neomycin gene replaced part of exon 2 and intron 2. The neomycin sequences were fused in-frame to the coding sequence of the gene. Northern blot analysis detected a truncated fusion transcript in homozygous mice. Enzyme activity assays demonstrated a lack of functional ADPRT1 protein in homozygous mice.