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Genomic characteristics of RARRES1 wild type and knockout mice lung tissues

ABSTRACT: Genomic characteristics of RARRES1 wild type and knockout mice lung tissues

PROVIDER: PRJNA542797 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR9051630_1.fastq.gz	Fastqsanger.gz
	SRR9051630_2.fastq.gz	Fastqsanger.gz
	SRR9051640_1.fastq.gz	Fastqsanger.gz
	SRR9051640_2.fastq.gz	Fastqsanger.gz
	SRR9051631_1.fastq.gz	Fastqsanger.gz

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Genomic characteristics of RARRES1 wild type and knockout mice lung tissues

Project description:Purpose: RARRES1 is proposed as tumor suppressor gene but its function is not clear yet. To elucidate RARRES1 function in carcinogenesis, we examine phenotype and genetic characteristics of the RARRES1 genetically knockout mice lung. Methods: Genetic profiles of RARRES1 wild type and knockout mouse lung tissues of embryonic day 19.5, 10-month-old, and 18-month-old mice were analyzed by whole genome and RNA sequencing in triplicate, using Illumina Hiseq X ten. Additionally, three lung tumors originated from RARRES1 knockout mice also examine using same platform. Results: RARRES1 knockout accelerate spontaneous lung carcinogenesis, with pluripotency of stem cells, Hippo signaling pathway, Wnt signaling pathway, and cell cycle related genes are significantly activated including Nanog, CDK1, Cyclin E. In addition, RARRES1 knockout induced lung cancer had rare oncogenic mutations, on the contrary, lung tissue progenitor cell, lung bipotent progenitor cell and AT2 type cell popularity increased. Conclusions: RARRES1 knockout accelerate spontaneous lung carcinogenesis through organ stem cell population enhancement with various stemness related gene set activation beside rare mutational driving.

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Project description:The genetic defect underlying the human Smith-Lemli-Opitz dysmorphological disorder is loss-of-function mutations affecting the cholesterol synthesis enzyme dehydrocholesterol delta7 reductase, DHCR7. Dhcr7 knockout mice recapitulate the biochemical characteristics, but all knockout pups die within 14h of birth. Tissues of knockout mice accumulate the precursor sterol, 7-dehydrocholesterol, and show reduced levels of cholesterol (J. Clin. Invest. (2001) 108: 905-915). We compared the global gene expression changes in lung, liver and brain from knockout mice to those seen from organs harvested from same-pregnancy wild-type embryos, harvested before birth (E18.5). Since the P0 knockout pups die, we expected that there would be significant changes in gene expression between knockout and wild-type organs, and further comparing the altered genes in common to brain, lung and liver would point to a common mechanistic pathway where disruption of normal sterol synthesis in all cells leads to pathophysiology. Remarkably, these data show that the global gene expression between knockout and wild-type organs is hardly altered, despite the complete loss of cholesterol synthesis. There are so few genes that are altered, and furthermore, those that are altered are very limited in sharing similarities in all three tissues. This suggests that disorganized gene expression is not the cause of the early neonatal lethality.

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