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Mus musculus

ABSTRACT: Loss of the Melanocortin 4 Receptor in mice causes dilated cardiomyopathy.

PROVIDER: PRJNA385096 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR5494680_1.fastq.gz	Fastqsanger.gz
	SRR5494680_2.fastq.gz	Fastqsanger.gz
	SRR5494671_1.fastq.gz	Fastqsanger.gz
	SRR5494671_2.fastq.gz	Fastqsanger.gz
	SRR5494672_1.fastq.gz	Fastqsanger.gz

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Loss of the Melanocortin 4 Receptor in mice causes dilated cardiomyopathy.

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Project description:A novel ppp1r13l sequence variation causes dilated cardiomyopathy and cardiac inflammation. This experiment explores the transcriptome of wa3 mice hearts which are carry deletion and insertion mutations in exon 12 of the Ppp1r13l gene that generate premature stop codon, and exhibit dilated cardio myopathy in a similar manner to a novel human mutation that was recently dicovered.

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Project description:Nuclear envelope (NE) ruptures are emerging observations in Lamin-related dilated cardiomyopathy, an adult-onset disease caused by loss-of-function mutations in Lamin A/C, a nuclear lamina component. Here, we test a prevailing hypothesis that NE ruptures trigger the pathological cGAS-STING cytosolic DNA-sensing pathway using a mouse model of Lamin cardiomyopathy. The reduction of Lamin A/C in cardiomyocytes of adult mice causes pervasive NE ruptures in cardiomyocytes, preceding inflammatory transcription, fibrosis, and fatal dilated cardiomyopathy. NE ruptures are followed by DNA damage accumulation without causing immediate cardiomyocyte death. However, cGAS-STING-dependent inflammatory signaling remains inactive. Deleting cGas or Sting does not rescue cardiomyopathy. The lack of cGAS-STING activation is likely due to the near absence of cGAS expression in adult cardiomyocytes at baseline. Instead, extracellular matrix (ECM) signaling is activated and predicted to initiate pro-inflammatory communication from Lamin-reduced cardiomyocytes to fibroblasts. Our work nominates ECM signaling, not cGAS-STING, as a potential inflammatory contributor in Lamin cardiomyopathy.

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Bidirectional Introgression between Mus musculus domesticus and Mus spretus.

Project description:Introgressed variants from other species can be an important source of genetic variation because they may arise rapidly, can include multiple mutations on a single haplotype, and have often been pretested by selection in the species of origin. Although introgressed alleles are generally deleterious, several studies have reported introgression as the source of adaptive alleles-including the rodenticide-resistant variant of Vkorc1 that introgressed from Mus spretus into European populations of Mus musculus domesticus. Here, we conducted bidirectional genome scans to characterize introgressed regions into one wild population of M. spretus from Spain and three wild populations of M. m. domesticus from France, Germany, and Iran. Despite the fact that these species show considerable intrinsic postzygotic reproductive isolation, introgression was observed in all individuals, including in the M. musculus reference genome (GRCm38). Mus spretus individuals had a greater proportion of introgression compared with M. m. domesticus, and within M. m. domesticus, the proportion of introgression decreased with geographic distance from the area of sympatry. Introgression was observed on all autosomes for both species, but not on the X-chromosome in M. m. domesticus, consistent with known X-linked hybrid sterility and inviability genes that have been mapped to the M. spretus X-chromosome. Tract lengths were generally short with a few outliers of up to 2.7 Mb. Interestingly, the longest introgressed tracts were in olfactory receptor regions, and introgressed tracts were significantly enriched for olfactory receptor genes in both species, suggesting that introgression may be a source of functional novelty even between species with high barriers to gene flow.

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Project description:Gene expression profiling on mouse models of dilated cardiomyopathy

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