Dataset Information

Zebrafinch Blood Proteome - BetaA, the major beta globin in definitive red blood cells, is present from the onset of primitive erythropoiesis in chicken

ABSTRACT: Not available

INSTRUMENT(S): instrument model, LTQ

ORGANISM(S): Taeniopygia Guttata (zebra Finch) (poephila Guttata)

TISSUE(S): Blood Cell, Embryonic Blood, Blood, Hematopoietic Cell

SUBMITTER: Cantas Alev

PROVIDER: PRD000099 | Pride | 2010-04-29

REPOSITORIES: Pride

ACCESS DATA

Dataset's files

Source:

			Action	DRS
	PRIDE_Exp_Complete_Ac_9204.pride.mgf.gz	Mgf
	PRIDE_Exp_Complete_Ac_9204.xml.gz	Xml
	PRIDE_Exp_Complete_Ac_9205.pride.mgf.gz	Mgf
	PRIDE_Exp_Complete_Ac_9205.xml.gz	Xml
	PRIDE_Exp_Complete_Ac_9206.pride.mgf.gz	Mgf

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Publications

Genomic organization of zebra finch alpha and beta globin genes and their expression in primitive and definitive blood in comparison with globins in chicken.

Alev Cantas C Shinmyozu Kaori K McIntyre Brendan A S BA Sheng Guojun G

Development genes and evolution 20090716 7

How alpha and beta globin genes are organized and expressed in amniotes is of interest to researchers in a wide variety of fields. Data regarding this from avian species have been scarce. Using genomic and proteomic approaches, we present here our analysis of alpha and beta globins of zebra finch, a passerine bird. We show that finch alpha globin gene cluster has three genes (alphas 1-3), each orthologous to its chicken counterpart. Finch beta globin gene cluster has three genes (betas 1-3), wit ...[more]

PMID: 19609557

Publication: 1/2

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Project description:Congenital dyserythropoietic anemia type I (CDA I) is an autosomal recessive disease characterized by moderate to severe macrocytic anemia and pathognomonic morphologic abnormalities of the erythroid precursors, including spongy heterochromatin. The disease is mainly caused by mutations in CDAN1 (encoding for Codanin-1). No patients with homozygous null type mutations have been described, and mouse null mutants die during early embryogenesis prior to the initiation of erythropoiesis. The cellular functions of Codanin-1 and the erythroid specificity of the phenotype remain elusive. To investigate the role of Codanin-1 in erythropoiesis, we crossed mice carrying the Cdan1 floxed allele (Cdan fl/fl ) with mice expressing Cre-recombinase under regulation of the erythropoietin receptor promoter (ErGFPcre). The resulting CdanΔEry transgenic embryos died at mid-gestation (E12.5-E13.5) from severe anemia, with very low numbers of circulating erythroblast. Transmission electron microscopy studies of primitive erythroblasts (E9.5) revealed the pathognomonic spongy heterochromatin. The morphology of CdanΔEry primitive erythroblasts demonstrated progressive development of dyserythropoiesis. Annexin V staining showed increases in both early and late-apoptotic erythroblasts compared to controls. Flow cytometry studies using the erythroid-specific cell-surface markers CD71 and Ter119 demonstrated that CdanΔEry erythroid progenitors do not undergo the semi-synchronous maturation characteristic of primitive erythroblasts. Gene expression studies aimed to evaluate the effect of Cdan1 depletion on erythropoiesis revealed a delay of ζ to α globin switch compared to controls. We also found increased expression of Gata2, Pu.1, and Runx1, which are known to inhibit terminal erythroid differentiation. Consistent with this data, our zebrafish model showed increased gata2 expression upon cdan1 knockdown. In summary, we demonstrated for the first time that Cdan1 is required for primitive erythropoiesis, while providing two experimental models for studying the role of Codanin-1 in erythropoiesis and in the pathogenesis of CDA type I.