All Phenotypes Parp1<tm1Zqw> MGI Mouse

Phenotypes associated with this allele

Jump to	Allelic Composition	Genetic Background	Genotype ID
hm1	Parp1^tm1Zqw/Parp1^tm1Zqw	129S-Parp1^tm1Zqw/J	MGI:4367617
hm2	Parp1^tm1Zqw/Parp1^tm1Zqw	involves: 129S2/SvPas	MGI:5556092
hm3	Parp1^tm1Zqw/Parp1^tm1Zqw	involves: 129S2/SvPas * C57BL/6	MGI:3511156
hm4	Parp1^tm1Zqw/Parp1^tm1Zqw	involves: 129/Sv * C57BL/6	MGI:3513073
cx5	Brca1^tm2.1Cxd/Brca1^tm2.1Cxd Parp1^tm1Zqw/Parp1^tm1Zqw	involves: 129S2/SvPas * 129S6/SvEvTac	MGI:4360485

♀	phenotype observed in females
♂	phenotype observed in males
N	normal phenotype

nervous system

decreased neuron apoptosis ( J:96548 )

• wild-type neurons co-cultured with microglial cells exposed to TFN-alpha exhibit decreased cell death compared to neurons co-cultured with similarly treated wild-type microglial cells

abnormal microglial cell physiology ( J:96548 )

• TNF-alpha fails to activate microglial cells unlike in similarly treated wild-type microglia

• LPS activation of microglial cells is suppressed compared with similarly treated wild-type cells

homeostasis/metabolism

decreased circulating creatinine level ( J:95418 )

• at 1-3 days post-renal I/R injury, serum creatinine levels are significantly reduced relative to those in similarly treated wild-type controls

abnormal response/metabolism to endogenous compounds ( J:96548 )

• TNF-alpha fails to activate microglial cells unlike in similarly treated wild-type microglia

decreased physiological sensitivity to xenobiotic ( J:96548 )

• LPS activation of microglial cells is suppressed compared with similarly treated wild-type cells

decreased susceptibility to kidney reperfusion injury ( J:95418 )

• following renal ischemic reperfusion (I/R) injury, homozygotes show significantly attenuated tubular cast formation, cellular necrosis, and red cell trapping in the corticomedullary region (day 1), and a significantly reduced number of dilated tubules (day 5) relative to similarly treated wild-type controls

• at 6, 12, and 24 hrs post I/R injury, kidney ATP levels are 80%, 73%, and 77%, respectively, of those in sham-operated controls, unlike in postischemic wild-type kidneys where ATP levels decline to 28%, 26%, and 43%

• however, no differences in the mortality rate, ROS levels, or number of nuclei with DNA strand breaks in proximal tubules are observed relative to wild-type controls

immune system

abnormal microglial cell physiology ( J:96548 )

• TNF-alpha fails to activate microglial cells unlike in similarly treated wild-type microglia

• LPS activation of microglial cells is suppressed compared with similarly treated wild-type cells

decreased inflammatory response ( J:95418 )

• following renal I/R injury, homozygotes exhibit decreased neutrophil infiltration (at 6, 12, and 24 hrs) and reduced expression of TNF-alpha, IL-1beta, and ICAM-1 (at 12 and 24 hrs) relative to similarly treated wild-type controls

cellular

decreased renal tubule apoptosis ( J:95418 )

• at 12 hrs post I/R injury, the number of apoptotic (TUNEL+) proximal tubule cells in the outer medulla is significantly decreased relative to that in similarly treated wild-type kidneys

decreased neuron apoptosis ( J:96548 )

• wild-type neurons co-cultured with microglial cells exposed to TFN-alpha exhibit decreased cell death compared to neurons co-cultured with similarly treated wild-type microglial cells

renal/urinary system

decreased renal tubule apoptosis ( J:95418 )

• at 12 hrs post I/R injury, the number of apoptotic (TUNEL+) proximal tubule cells in the outer medulla is significantly decreased relative to that in similarly treated wild-type kidneys

decreased susceptibility to kidney reperfusion injury ( J:95418 )

• however, no differences in the mortality rate, ROS levels, or number of nuclei with DNA strand breaks in proximal tubules are observed relative to wild-type controls

increased renal glomerular filtration rate ( J:95418 )

• at 24 hrs post-renal I/R injury, GFR is significantly augmented relative to that in similarly treated wild-type controls

hematopoietic system

abnormal microglial cell physiology ( J:96548 )

• TNF-alpha fails to activate microglial cells unlike in similarly treated wild-type microglia

• LPS activation of microglial cells is suppressed compared with similarly treated wild-type cells

Allelic Composition	Parp1^tm1Zqw/Parp1^tm1Zqw
Genetic Background	involves: 129S2/SvPas

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Parp1^tm1Zqw mutation (3 available); any Parp1 mutation (65 available)

♀	phenotype observed in females
♂	phenotype observed in males
N	normal phenotype

immune system

immune system phenotype ( J:146533 )

N	• B cells exhibit no defect in IL4 rescue of cell death induced by death by neglect or after irradiation

Allelic Composition	Parp1^tm1Zqw/Parp1^tm1Zqw
Genetic Background	involves: 129S2/SvPas * C57BL/6

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Parp1^tm1Zqw mutation (3 available); any Parp1 mutation (65 available)

♀	phenotype observed in females
♂	phenotype observed in males
N	normal phenotype

cellular

decreased neuron apoptosis ( J:65747 )

• homozygotes are resistant to apoptosis typically induced by monocular deprivation in the dorsal lateral geniculate nucleus (dLGN)

• in wild-type mice, monocular deprivation causes Trp53 accumulation, cell death, and progressive neuronal loss in the dLGN, with an early accumulation of citrulline

decreased susceptibility to dopaminergic neuron neurotoxicity ( J:23942 )

• homozygotes exhibit reduced susceptibility to damage induced by neurotoxin 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)

decreased cell proliferation ( J:23942 )

• mutant mouse embryonic fibroblasts (MEFs) are able to efficiently repair DNA damaged by UV and alkylating agents

• however, mutant MEFs exhibit a reduced proliferation rate relative to wild-type MEFs

• in addition, mutant thymocyte progenitors show impaired proliferation and a slow recovery following whole-body gamma-radiation

homeostasis/metabolism

decreased susceptibility to dopaminergic neuron neurotoxicity ( J:23942 )

• homozygotes exhibit reduced susceptibility to damage induced by neurotoxin 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)

nervous system

decreased neuron apoptosis ( J:65747 )

• homozygotes are resistant to apoptosis typically induced by monocular deprivation in the dorsal lateral geniculate nucleus (dLGN)

• in wild-type mice, monocular deprivation causes Trp53 accumulation, cell death, and progressive neuronal loss in the dLGN, with an early accumulation of citrulline

decreased susceptibility to dopaminergic neuron neurotoxicity ( J:23942 )

• homozygotes exhibit reduced susceptibility to damage induced by neurotoxin 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)

integument

skin hyperplasia ( J:23942 )

• homozygotes are viable, fertile, of normal size, and do not display any gross physical or behavioral abnormalities

• older homozygotes are susceptible to spontaneous development of skin disease: ~30% of older mice develop epidermal hyperplasia

Allelic Composition	Parp1^tm1Zqw/Parp1^tm1Zqw
Genetic Background	involves: 129/Sv * C57BL/6

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Parp1^tm1Zqw mutation (3 available); any Parp1 mutation (65 available)

♀	phenotype observed in females
♂	phenotype observed in males
N	normal phenotype

immune system

decreased inflammatory response ( J:94497 )

• neutrophil infiltration was prevented in TNBS treated mutant mice but not in wild-type

homeostasis/metabolism

enhanced wound healing ( J:94172 , J:94497 )

• induction of colitis resulted in reduced epithelial apoptosis in inflamed colon and faster resolution of colon damage compared to wild-type (J:94172)

• induction of colitis with rinitrobenzenesulfonic acid (TNBS) resulted in mucosal congestion, erosion, and hemorrhagic ulcerations of the distal colon and rectum in both wild-type and mutants, however the damage started to resolve after 72 hours and by 6-7 days, tissues were normal in mutants but damage was maintained in wild-type (J:94497)

• induction of colitis caused only 20% of mutant mice to develop serious diarrhea and to die within 48 hours compared to 100% of wild-type developing diarrhea and 50% dying (J:94497)

decreased susceptibility to injury ( J:94172 )

• reduced plasma levels of nitrite/nitrate when colitis was induced

Allelic Composition	Brca1^tm2.1Cxd/Brca1^tm2.1Cxd Parp1^tm1Zqw/Parp1^tm1Zqw
Genetic Background	involves: 129S2/SvPas * 129S6/SvEvTac

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Brca1^tm2.1Cxd mutation (1 available); any Brca1 mutation (113 available)
Parp1^tm1Zqw mutation (3 available); any Parp1 mutation (65 available)

♀	phenotype observed in females
♂	phenotype observed in males
N	normal phenotype

mortality/aging

lethality throughout fetal growth and development, complete penetrance ( J:139260 )

• death occurs between E12.5 and E15.5

• no double homozygotes survive beyond E15.5

growth/size/body

decreased embryo size ( J:139260 )

• embryos are significantly smaller than normal

• development is apparently normal until death occurs between E12.5 and E15.5

nervous system

exencephaly ( J:139260 )

• in about 1/3 of homozygotes

• failure of anterior neural tube to close

• elevated apoptosis in the neuroepithelium

cellular

abnormal centrosome morphology ( J:139260 )

• 40% of MEFs with more than 2 centrosomes

abnormal chromosome morphology ( J:139260 )

• quadriradial stuctures in metaphase

aneuploidy ( J:139260 )

• 45% of MEFs display aneuploidy

decreased telomere length ( J:139260 )

• MEFs have shortened telomeres

decreased cell proliferation ( J:139260 )

• poor growth of MEFs derived at E14.5

embryo

decreased embryo size ( J:139260 )

• embryos are significantly smaller than normal

• development is apparently normal until death occurs between E12.5 and E15.5

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