The phenotype of FancB-mutant mouse embryonic stem cells

Tae Moon Kim, Jun Ho Ko, Yong Jun Choi, Lingchuan Hu, Paul Hasty

Research output: Contribution to journalArticlepeer-review

14 Scopus citations


Fanconi anemia (FA) is a rare autosomal recessive disease characterized by bone marrow failure, developmental defects and cancer. There are multiple FA genes that enable the repair of interstrand crosslinks (ICLs) in coordination with a variety of other DNA repair pathways in a way that is poorly understood. Here we present the phenotype of mouse embryonic stem (ES) cells mutated for FancB. We found FancB-mutant cells exhibited reduced cellular proliferation, hypersensitivity to the crosslinking agent mitomycin C (MMC), increased spontaneous and MMC-induced chromosomal abnormalities, reduced spontaneous sister chromatid exchanges (SCEs), reduced gene targeting, reduced MMC-induced Rad51 foci and absent MMC-induced FancD2 foci. Since FancB is on the X chromosome and since ES cells are typically XY, FancB is an excellent target for an epistatic analysis to elucidate FA's role in ICL repair.

Original languageEnglish (US)
Pages (from-to)20-27
Number of pages8
JournalMutation Research - Fundamental and Molecular Mechanisms of Mutagenesis
Issue number1-2
StatePublished - Jul 1 2011


  • FancD2
  • Fanconi anemia
  • G2 arrest
  • Interstrand crosslink
  • Rad51
  • Radial

ASJC Scopus subject areas

  • Molecular Biology
  • Genetics
  • Health, Toxicology and Mutagenesis


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