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Severe Fanconi Anemia phenotypes in Fancd2 depletion mice.

Abstract：

:Fanconi anemia (FA) is a genetic disorder characterized by congenital malfunction, bone marrow failure and hypersensitivity to DNA damage. FANCD2 protein play the central role in FA pathway. To study the in vivo role of FANCD2, we generated and characterized a new Fancd2 knockout mouse strain with 7bp deletion in Fancd2 gene 5' terminus using Crispr-Cas9 in congenic C57BL/6J background. This Fancd2-/- mice displayed similar but overall more severe manifestation than the previous ES cell targeted Fancd2 model. These features include increased embryonic and postnatal lethality rate, higher incidence of microphthalmia, and more severe hypogonadism. The anemia we observed in this Fancd2-/- mice has not been described in other FA models. Further study indicated that the hematopoiesis deficiency was associated with increased apoptotic cell death, G2/M phase arrest and hypersensitivity to MMC and IR damage of Fancd2-/- bone marrow progenitor cells. Collectively, the resulting Fancd2-/- mice with higher resemblance of FA patient symptoms, will be useful in understand the parthenogenesis of pancytopenia and bone marrow failure in FA.

journal_name

Biochem Biophys Res Commun

journal_title

Biochemical and biophysical research communications

authors

Yang Q,Xie H,Zhong Y,Li D,Ke X,Ying H,Yu B,Zhang T

doi

10.1016/j.bbrc.2019.04.201

subject

Has Abstract

pub_date

2019-06-30 00:00:00

pages

713-719

issue

3

eissn

0006-291X

issn

1090-2104

pii

S0006-291X(19)30866-6

journal_volume

514

pub_type

杂志文章

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