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Lack of major genome instability in tumors of p53 null rats

ABSTRACT: Lack of major genome instability in tumors of p53 null rats

PROVIDER: PRJEB5836 | ENA |

REPOSITORIES: ENA

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			Action	DRS
		Other
	ERR455192.fastq.gz	Fastqsanger.gz
	ERR455193.fastq.gz	Fastqsanger.gz
	ERR455195.fastq.gz	Fastqsanger.gz
	ERR455197.fastq.gz	Fastqsanger.gz

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Lack of major genome instability in tumors of p53 null rats.

Project description:Tumorigenesis is often associated with loss of tumor suppressor genes (such as TP53), genomic instability and telomere lengthening. Previously, we generated and characterized a rat p53 knockout model in which the homozygous rats predominantly develop hemangiosarcomas whereas the heterozygous rats mainly develop osteosarcomas. Using genome-wide analyses, we find that the tumors that arise in the heterozygous and homozygous Tp53C273X mutant animals are also different in their genomic instability profiles. While p53 was fully inactivated in both heterozygous and homozygous knockout rats, tumors from homozygous animals show very limited aneuploidy and low degrees of somatic copy number variation as compared to the tumors from heterozygous animals. In addition, complex structural rearrangements such as chromothripsis and breakage-fusion-bridge cycles were never found in tumors from homozygous animals, while these were readily detectable in tumors from heterozygous animals. Finally, we measured telomere length and telomere lengthening pathway activity and found that tumors of homozygous animals have longer telomeres but do not show clear telomerase or alternative lengthening of telomeres (ALT) activity differences as compared to the tumors from heterozygous animals. Taken together, our results demonstrate that host p53 status in this rat p53 knockout model has a large effect on both tumor type and genomic instability characteristics, where full loss of functional p53 is not the main driver of large-scale structural variations. Our results also suggest that chromothripsis primarily occurs under p53 heterozygous rather than p53 null conditions.

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RNAseq expression of p53-null and p53-null/PLK2-null mammary tumors

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Project description:Seeds, including soybean (Glycine max), contain bioactive proteins with anti-nutritional and immunological properties that affect metabolism and assimilation of seed derived nutrients and as allergens that can induce escalating adverse immune responses. The presence of anti-nutritional proteins requires soybean protein to be processed by heat that results in energy costs and alteration of soybean protein’s physiochemical properties. Nulls for bioactive seed proteins have been isolated from the USDA soybean collection including Kunitz trypsin inhibitor (TI) and soybean agglutinin (LE) and immunodominant soybean allergen P34 proteins. Each of these nulls has the potential to partially address concerns of soybean feed/food consumption and stacked together these traits can form a basis for engineering improved soybean cultivars. A stack of cultivars of recessive nulls of TI, LE, and P34 was created in a cv Williams 82 background termed “Triple Null”. The reduction of these proteins slightly diminishes the overall protein content of the seed that was analyzed by 2D IEF/SDS gels and proteomics. P34 and Kunitz Trypsin Inhibitor nulls are frame shift mutants shown by mass spectroscopy to accumulate small amounts of authentic protein. Triple Null’s capacity for biolistic transformation was assessed showing that Triple Null can be transformed permitting stacking of transgene traits. Triple Null has possible application as a conventional feed/food source and for immunotherapy to mitigate soybean allergenic response and be leveraged as a transformation platform to stack other production or consumer traits.

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Project description:We performed an RNA-Seq analysis comparing thymic lymphoma tissues from the p53-null(n=2) and ΔNp63Δ/Δ;p53-/- (n=3) or ΔNp73Δ/Δ;p53-/-(n=3). Mice at 10 weeks of age were injected with either Ad-mCherry or Ad-CRE-mCherry to delete ΔNp63/ΔNp73 in the thymic lmyphomas. We aimed to test by deleting the DNp63/DNp73 in these p53-deficient tumors will mediate tumor regression and analyze the expression profile of the genes

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