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129-derived passenger mutations confound phenotype of ACKR1-deficient mice

ABSTRACT: 129-derived passenger mutations confound phenotype of ACKR1-deficient mice

PROVIDER: PRJNA1077396 | ENA |

REPOSITORIES: ENA

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129-derived passenger mutations confound phenotype of ACKR1-deficient mice

Project description:A majority of genetically modified mice carry passenger mutations, originating from the 129-derived embryonic stem (ES) cells, near the targeted gene. Unintended retention of these mutations can introduce confounding phenotypes and affect conclusions. We show that Ackr1-/-129ES mice retained approximately 6 Mb of 129 ES cells-derived genomic material in chromosome 1 near Ackr1 in bone marrow derived monocytes (Mono), nucleated erythroblasts (NECs), and polymorphonucleated neutrophils (PMN), notably affecting the expression of PYHIN genes.

2024-09-15 | GSE256021 | GEO

Passenger Mutations Confound Phenotypes of SARM1-Deficient Mice.

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Passenger Mutations Confound Interpretation of All Genetically Modified Congenic Mice.

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Transcriptome of soleus muscle of Tenascin-C deficient 129/SV mice

Project description:1 year-old male Tenascin-C deficient 129/SV mice with the targeted insertion of a beta-lactamase cassette in the NcoI site of exon 2 of the TNC gene (Forsberg, E., Hirsch, E., Frohlich, L., Meyer, M., Ekblom, P., Aszodi, A., Werner, S. & Fassler, R. (1996) Proc. Natl. Acad. Sci U. S. A 93, 6594-6599) were used for the study. Animals were derived from the original strain and back-crossed with wildtype 129/SV mice (Institut für Labortierkunde, University of Zurich). Animals were acclimatized to housing in single cages for one week. Soleus muscle was harvested, total RNA isolated and subjected to transcript profiling with custom microarrays with custom-designed ATLASTM cDNA nylon filter as described (Dapp, C., Schmutz, S., Hoppeler, H. & Fluck, M. (2004) Physiol Genomics 20, 97-107). Keywords: Transcriptome

2008-08-08 | GSE8550 | GEO

Transcriptome of reloaded soleus muscle of Tenascin-C deficient 129/SV mice

Project description:1 year-old male Tenascin-C deficient 129/SV mice with the targeted insertion of a beta-lactamase cassette in the NcoI site of exon 2 of the TNC gene (Forsberg, E., Hirsch, E., Frohlich, L., Meyer, M., Ekblom, P., Aszodi, A., Werner, S. & Fassler, R. (1996) Proc. Natl. Acad. Sci U. S. A 93, 6594-6599) were used for the study. Animals were derived from the original strain and back-crossed with wildtype 129/SV mice (Institut für Labortierkunde, University of Zurich). Animals were acclimatized to housing in single cages for one week followed by 7 days of hindlimb suspension and one day of reloading. Soleus muscle was harvested, total RNA isolated and subjected to transcript profiling with custom microarrays with custom-designed ATLASTM cDNA nylon filter as described (Dapp, C., Schmutz, S., Hoppeler, H. & Fluck, M. (2004) Physiol Genomics 20, 97-107). Keywords: Transcriptome

2008-08-08 | GSE8551 | GEO

Transcriptome of soleus muscle of Tenascin-C deficient 129/SV mice

Project description:1 year-old male Tenascin-C deficient 129/SV mice with the targeted insertion of a beta-lactamase cassette in the NcoI site of exon 2 of the TNC gene (Forsberg, E., Hirsch, E., Frohlich, L., Meyer, M., Ekblom, P., Aszodi, A., Werner, S. & Fassler, R. (1996) Proc. Natl. Acad. Sci U. S. A 93, 6594-6599) were used for the study. Animals were derived from the original strain and back-crossed with wildtype 129/SV mice (Institut fÃ¼r Labortierkunde, University of Zurich). Animals were acclimatized to housing in single cages for one week. Soleus muscle was harvested, total RNA isolated and subjected to transcript profiling with custom microarrays with custom-designed ATLASTM cDNA nylon filter as described (Dapp, C., Schmutz, S., Hoppeler, H. & Fluck, M. (2004) Physiol Genomics 20, 97-107). Keywords: Transcriptome Seven biological replicas

2010-06-25 | E-GEOD-8550 | biostudies-arrayexpress

Effect of chemotherapy on passenger mutations in metastatic colorectal cancer

Project description:Effect of chemotherapy on passenger mutations in metastatic colorectal cancer

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Effect of chemotherapy on passenger mutations in metastatic colorectal cancer

Project description:Effect of chemotherapy on passenger mutations in metastatic colorectal cancer

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Transcriptome of reloaded soleus muscle of Tenascin-C deficient 129/SV mice

Project description:1 year-old male Tenascin-C deficient 129/SV mice with the targeted insertion of a beta-lactamase cassette in the NcoI site of exon 2 of the TNC gene (Forsberg, E., Hirsch, E., Frohlich, L., Meyer, M., Ekblom, P., Aszodi, A., Werner, S. & Fassler, R. (1996) Proc. Natl. Acad. Sci U. S. A 93, 6594-6599) were used for the study. Animals were derived from the original strain and back-crossed with wildtype 129/SV mice (Institut fÃ¼r Labortierkunde, University of Zurich). Animals were acclimatized to housing in single cages for one week followed by 7 days of hindlimb suspension and one day of reloading. Soleus muscle was harvested, total RNA isolated and subjected to transcript profiling with custom microarrays with custom-designed ATLASTM cDNA nylon filter as described (Dapp, C., Schmutz, S., Hoppeler, H. & Fluck, M. (2004) Physiol Genomics 20, 97-107). Keywords: Transcriptome Six biological replicas

2010-06-25 | E-GEOD-8551 | biostudies-arrayexpress

Genomic contamination causes NLRP1 hypersensitivity and altered cell surface markerGenomic contamination causes NLRP1 hypersensitivity and altered cell surface marker expression in Nlrp3-/- macrophagesGenomic contamination causes NLRP1 hypersensitivity and altered cell surface marker expression in Nlrp3-/- macrophages

Project description:The NLRP1 and NLRP3 inflammasomes are critical immune signaling hubs that drive cytokine release and inflammatory cell death, and have been implicated in the pathogenesis of diverse diseases. Much of our understanding of inflammasome biology stems from experiments performed in transgenic mouse lines. However, the unavoidable retention of highly polymorphic genomic regions in transgenic mice can confound results, leading to false conclusions, and delaying scientific progress and clinical development. Here, we found that the most commonly used NLRP3 deficient mouse strain, unknowingly contains a substantial region of 129 genome proximal to Nlrp3, causing a hypersensitive response to NLRP1 stimulation, altered gene regulation across multiple cell-types, and the misexpression of the key macrophage cell surface marker TIM4, independently of NLRP3 deficiency. Our results demonstrate that phenotypes previously attributed to the loss of NLRP3 expression may in fact be a byproduct of passenger mutations, and that conventional macrophage identification is obsolete. These data, and our validation of a previously unreported conditional Nlrp3 allele, are critical for the immunology community in ensuring correct data interpretation and improving experimental design. Furthermore, they open new questions in how genetically distinct mouse strains regulate inflammasome protein stability and expression to restrict excessive inflammation.

2024-09-16 | PXD046782 | Pride

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