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Next Generation Sequencing Facilitates Quantitative Analysis of B73 and zmuvr8-1 mutant in low white with or without UVB treat Transcriptomes

ABSTRACT: Next Generation Sequencing Facilitates Quantitative Analysis of B73 and zmuvr8-1 mutant in low white with or without UVB treat Transcriptomes

PROVIDER: PRJNA1002251 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR25520047_1.fastq.gz	Fastqsanger.gz
	SRR25520047_2.fastq.gz	Fastqsanger.gz
	SRR25520048_1.fastq.gz	Fastqsanger.gz
	SRR25520048_2.fastq.gz	Fastqsanger.gz
	SRR25520049_1.fastq.gz	Fastqsanger.gz

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Next Generation Sequencing Facilitates Quantitative Analysis of B73 and zmuvr8-1 mutant in low white with or without UVB treat Transcriptomes

Project description:Analysis of differential gene expression regulated by UVB. The hypothesis tested in the present study was that ZmUVR8 mediates mostly UVB regulated genes' expression

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Project description:Skin cancer is the most prevalent cancer in humans, especially in the United States, Australia, and New Zealand. Australia and New Zealand are the two countries with the highest rates of skin cancer in the world, about four times higher than the United States, the United Kingdom and Canada. According to statistics, one American dies of skin cancer every hour. Studies have shown that ultraviolet radiation is the main cause of skin cancer, and ultraviolet rays are mainly divided into UVA, UVB and UVC according to wavelength, UVA and UVB can cause DNA damage, and UVB is the main factor that induces skin cancer. UVB is primarily a direct damage to cellular DNA and generally includes the formation of pyrimidine dimers (CPDs) and 6-4 photoproducts (6-4PPs). UVB can also cause mutations in tumor suppressor genes such as p53, ptch, and ras. These bases the mutation will promote the activation of related signaling pathways, thereby inducing the production of tumors.In this study, we will use gene chip technology to screen out UVB-sensitive genes, and then select the genes of the UVB-sensitive GPCR family from these genes, and further use PCR for verification, so as to identify UVB-sensitive GPCRs, which will provide a basis for further experimental research.

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Next Generation Sequencing Facilitates Quantitative Analysis of UVB(20mJ/cm2 and 40mJ/cm2) exposed and untreated HaCaT keratinocytes Transcriptomes

Project description:Purpose: To compare the transcriptomes of UVB (20mJ/cm2 and 40mJ/cm2) exposed and untreated HaCaT keratinocytes by RNA-Seq analysis, trying to find differences in gene expression between UVB exposed and untreated of keratinocytes and then elucidate the candidate genes that may play important roles in the differentiation of UVB-induced damage in keratinocytes. Methods: HaCaT keratinocytes were subjected to 20mJ/cm2 and 40mJ/cm2 UVB irradiation. Results: To better understand the effects of UVB (20 mJ/cm2), mRNA-sequecing (n=3) were completed by Novogene Inc. A total 891 differentially expressed genes (DEGs) were identified between UV group and control group with 604 down-regulated and 287 up-regulated. A total of 4036 differentially expressed genes (DEGs) which compared with untreated group were identified by RNA-Seq, which provided abundant data for further analysis.

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Project description:Previous studies showed that SV40 transformed cells have unique DNA damage responses; further inspecting these responses by microarray provides an opportunity to discover transciprtional insights of DNA damage responses after UVB irradiation. This study is used to comapre to GSE7589, our previous study of human normal lung fibroblast after UVB irradiation. We used a loop design in this study, cDNA microarray experiment consisted of eight RNA samples, including UVB-irradiated samples and their corresponding controls of 4 time points after UV irradiation.

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Project description:Considering that human skin cancer is predominantly attributed to UV radiation from sunlight, additional investigations are needed to elucidate the role of P2RY6 in UVB-induced skin carcinogenesis. Surprisingly, we find that P2ry6 deletion exhibits marked promotion to UVB-induced skin papilloma formation compared with wild-type mice, suggesting its tumor-suppressive role in UVB-induced skin cancer. Additionally, P2ry6 knockout promotes mouse skin hyperplasia induced by short-term UVB irradiation, while UDP, the ligand of P2RY6, can inhibit UVB-induced skin damage. Furthermore, UVB irradiation can significantly upregulate P2RY6 expression in mouse and human skin cells. These results indicate that P2RY6 plays a crucial protective role in resisting UVB-induced skin damage and carcinogenesis. At the molecular level, P2RY6 deletion inhibits ubiquitination and expression of XPC after UVB irradiation in keratinocytes, resulting in the accumulation of CPDs (cyclobutane pyrimidine dimers). P2RY6 deletion also activates PI3K/AKT signaling pathway in vitro and in vivo. The CPD accumulation and inflammatory responses enhanced by P2RY6 deletion are reversed by an AKT inhibitor. These findings suggest that P2RY6 acts as a tumor suppressor in UVB-induced skin cancer by regulating PI3K/AKT signaling pathway.

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