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RNA-seq for gata1+ cells in add1 mutant zebrafish embryos and siblings at 22 hpf

ABSTRACT: RNA-seq for gata1+ cells in add1 mutant zebrafish embryos and siblings at 22 hpf

PROVIDER: PRJNA991987 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR25181149_1.fastq.gz	Fastqsanger.gz
	SRR25181149_2.fastq.gz	Fastqsanger.gz
	SRR25181150_1.fastq.gz	Fastqsanger.gz
	SRR25181150_2.fastq.gz	Fastqsanger.gz

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RNA-seq for gata1+ cells in add1 mutant zebrafish embryos and siblings at 22 hpf

Project description:Adducin 1 (Add1) functions primarily as a membrane cytoskeletal protein, whereas Add1 contains a bipartite nuclear localization signal, implying its special nuclear function. However, the nuclear functional roles of Add1 apart from maintaining cytoskeletal stability remain unknown. Here, we created add1-deficient zebrafish using Tol2 transposon-mediated gene trapping and evaluated how add1 deficiency affected early hematopoiesis development. When add1 is lacking in zebrafish, both the primitive erythropoiesis and definitive hematopoiesis are compromised, and the primitive erythroblast cells are unable to develop into healthy erythrocytes. More significantly, the RNA sequencing results demonstrated that the p53 pathway is activated in the add1-depletion erythroblast cells, causing the erythroblasts to undergo apoptosis at the 14-somites stage and 24 hpf. Additionally, the anemic phenotype and apoptosis in add1-deficient embryos can be partially rescued by p53 insufficiency. Taken together, our findings show that add1 is critical for zebrafish erythropoiesis partially through the p53-mediated apoptotic pathway, which expands the regulatory role of Add1 for nuclear function.

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