Increased mutation in mice genetically predisposed to oxidative damage in the brain

Stringer, James R.; Larson, Jon S.; Fischer, Jared M.; Stringer, Saundra L.

doi:10.1016/j.mrfmmm.2004.07.010

Cited by 13 publications

(6 citation statements)

References 27 publications

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“…Under normal physiological conditions AIF plays an important physiological role in mitochondria (111,112). Studies using Aif knockout cells and Harlequin (Hq) mutant mice, which have only 20% AIF expression strongly suggested that AIF serves as a reactive oxygen species (ROS) scavenger (98,(111)(112)(113)(114)(115). Moreover, oxidative phosphorylation is compromised in cells with depleted AIF due to reduced expression of the electron transport chain complex I in the mitochondria (98,(111)(112)(113)(114)(115).…”

Section: Programmed-necrotic Cell Deathmentioning

confidence: 99%

“…Studies using Aif knockout cells and Harlequin (Hq) mutant mice, which have only 20% AIF expression strongly suggested that AIF serves as a reactive oxygen species (ROS) scavenger (98,(111)(112)(113)(114)(115). Moreover, oxidative phosphorylation is compromised in cells with depleted AIF due to reduced expression of the electron transport chain complex I in the mitochondria (98,(111)(112)(113)(114)(115). Recent data strongly indicate, that the redox-active enzymatic region of AIF is associated with anti-apoptotic functions, while its DNA binding region possesses proapoptotic/necrotic activities ( (105, 116) and reviewed in (117,118)).…”

Section: Programmed-necrotic Cell Deathmentioning

confidence: 99%

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The molecular "Jekyll and Hyde" duality of PARP1 in cell death and cell survival

Hassa¹

2009

Front Biosci

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The current literature clearly indicates that PARP1 but also PARP2 play a pivotal role in modulating the cellular responses to stress. Genetic and pharmacological studies demonstrated that overactivation of PARP1 is a key mediator of programmed-necrotic cell death in vivo. PARP1 appears to be also involved in programmed cell death processes others than necrosis, such as apoptosis or macroautophagocytotic cell death. On the other hand, growing evidence suggests that both PARP1 and PARP2 are multi-faced enzymes also playing important roles in cell survival processes. PARP1 and PARP2 were shown to be required for the maintenance of genomic integrity and to act as a survival factor for highly proliferating cells such as stem cells but also non-proliferating neuronal cells against cell death induced by oxidative stress under mild and moderate progressive damage in vivo. This review briefly summarizes the recent findings, which support a crucial role of PARP1 in different programmed cell death and cell survival processes. A special focus is placed on the proposed molecular mechanisms underlying the "Jekyll and Hyde" duality of PARP1 in cell death and cell survival pathways. A potential crosstalk between PARP1, PARP2 and other NAD+-dependent ADP-ribosyling enzymes such as Sirtuins and CD38 in cell death and survival pathways is discussed.

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Section: Programmed-necrotic Cell Deathmentioning

confidence: 99%

Section: Programmed-necrotic Cell Deathmentioning

confidence: 99%

The molecular "Jekyll and Hyde" duality of PARP1 in cell death and cell survival

Hassa¹

2009

Front Biosci

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“…It is reasonable to expect that expression of the transgene can be made more universal by placing it at the ROSA26 locus, which has been shown to support ubiquitous expression of a variety of transgenes (Soriano, 1999;Awatramani et al, 2001;Srinivas et al, 2001). The G11 PLAP mouse model can detect increased mutation in mice that exhibit mismatch repair deficiency, that have increased tumor incidence, that are subject to oxidative damage, that are treated with mutagenic chemicals Stringer et al, 2004Stringer et al, , 2005Fischer et al, 2005) and, in this study, aging. The G11 PLAP mouse model allows for the examination of the exact cell type that was mutated and proliferation postmutation.…”

Section: Discussionmentioning

confidence: 94%

“…The G11 PLAP mouse model offers the advantage of making it possible to see the mutant cells within a tissue, thereby revealing the types of cells that incur mutations (DePrimo et al ., 1996Cao et al ., 1998;Hersh et al ., 2002;Larson et al ., 2004;Stringer et al ., 2004Stringer et al ., , 2005Fischer et al ., 2005). G11 PLAP mice carry a mutant allele (G11) of a human Placental Alkaline Phosphatase (PLAP) transgene.…”

Section: Introductionmentioning

confidence: 99%

Mutation in aging mice occurs in diverse cell types that proliferate postmutation

Fischer

Stringer

2008

Aging Cell

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SummaryTo determine the relationship between aging, cell proliferation and mutation in different cell types, hearts, brains and kidneys from G11 PLAP mice between 1 week and 24 months of age were examined. Mutant cells were Regardless of tissue and cell type, PLAP + cells occurred as singletons and in clusters, both of which increased in frequency with age. These data show that age-associated accumulation of mutant cells occurs in diverse cell types and is due to both new mutation and proliferation of mutant cells, even in cell types that tend to not proliferate.

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“…In rare cases, microsatellite repeats exist in the coding regions of genes and may cause neurological disorders and cancer when frameshift occurs57. To date, there are a few mouse genetic studies that take advantage of mononucleotide repeat frameshift to study frameshift mutation rates in vivo 8910, or inducing mosaic Cre expression in intestinal cells1112. These studies did not reveal the potential of this approach for genetically directed sparse neuronal labeling, because the frameshift rate for G 11 repeat in the brain is about 10 −4 –10 −5 (Refs 8, 9, 10), which is much lower than the desirable sparse labeling frequency of about 1% neurons as in the classical Golgi method2.…”

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confidence: 99%

Genetically-directed Sparse Neuronal Labeling in BAC Transgenic Mice through Mononucleotide Repeat Frameshift

Yang

2017

Sci Rep

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Mosaicism with Repeat Frameshift (MORF) allows a single Bacterial Artificial Chromosome (BAC) transgene to direct sparse labeling of genetically-defined neuronal populations in mice. The BAC transgene drives cell-type-specific transcription of an out-of-frame mononucleotide repeat that is placed between a translational start codon and a membrane-bound fluorescent protein lacking its start codon. The stochastic frameshift of the unstable repeat DNA in a subset of BAC-expressing neurons results in the in-frame translation of the reporter protein hence the sparse neuronal labeling. As a proof-of-concept, we generated D1-dopamine receptor (D1) BAC MORF mice that label about 1% striatal D1-expressing medium spiny neurons and allow visualization of their dendrites. These mice enable the study of D1-MSN dendrite development in wildtype mice, and its degeneration in a mouse model of Huntington’s disease.

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Increased mutation in mice genetically predisposed to oxidative damage in the brain

Cited by 13 publications

References 27 publications

The molecular "Jekyll and Hyde" duality of PARP1 in cell death and cell survival

The molecular "Jekyll and Hyde" duality of PARP1 in cell death and cell survival

Mutation in aging mice occurs in diverse cell types that proliferate postmutation

Genetically-directed Sparse Neuronal Labeling in BAC Transgenic Mice through Mononucleotide Repeat Frameshift

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