Genomics

Dataset Information

28

Studies in an early development window unveils a severe HSC defect in both murine and human Fanconi anemia [human]


ABSTRACT: We performed a unique kinetics study of hematopoiesis in Fancg-/- mouse embryos, between E12.5 and E14.5 developmental window. We also report for the first time that a deep HSC defect is also observed during human FA development, and that human FA FL HSCs present a transcriptome profile similar to that of mouse E12.5 Fancg-/- FL HSCs. Overall design: Sorted CD34+CD38-CD45+CD117hi HSC-enriched population from a unique 13 WG Fanconi FL (FANCB)(n=1) and from control FL from fetuses at the same stage of development (i.e. second trimester, 13 and 17.7 WG) (n=2)were sorted and RNA was purified using RNeasy Plus Micro Kit (Qiagen). RNA concentration and integrity was evaluated with the Agilent Bioanalyzer 2100 and 2 ng of total RNA reverse transcribed following the Ovation Pico System V2 (Nugen). cDNA is then hybridized to GeneChip® HumanGene2.0ST (Affymetrix)

INSTRUMENT(S): [HuGene-2_0-st] Affymetrix Human Gene 2.0 ST Array [HuGene20stv1_Hs_ENTREZG_21.0.0]

SUBMITTER: Franck Letourneur  

PROVIDER: GSE120168 | GEO | 2018-11-30

REPOSITORIES: GEO

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Fanconi anemia (FA) causes bone marrow failure early during childhood, and recent studies indicate that a hematopoietic defect could begin in utero. We performed a unique kinetics study of hematopoiesis in Fancg<sup>-/-</sup> mouse embryos, between the early embryonic day 11.5 (E11.5) to E12.5 developmental window (when the highest level of hematopoietic stem cells [HSC] amplification takes place) and E14.5. This study reveals a deep HSC defect with exhaustion of proliferative and self-renewal c  ...[more]

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