Recent studies show overlap between Fanconi anemia (FA) proteins and those 
involved in DNA repair mediated by homologous recombination (HR). However, the 
mechanism by which FA proteins affect HR is unclear. FA proteins 
(FancA/C/E/F/G/L) form a multiprotein complex, which is responsible for DNA 
damage-induced FancD2 monoubiquitination, a key event for cellular resistance to 
DNA damage. Here, we show that FANCD2-disrupted DT40 chicken B-cell line is 
defective in HR-mediated DNA double-strand break (DSB) repair, as well as gene 
conversion at the immunoglobulin light-chain locus, an event also mediated by 
HR. Gene conversions occurring in mutant cells were associated with decreased 
nontemplated mutations. In contrast to these defects, we also found increased 
spontaneous sister chromatid exchange (SCE) and intact Rad51 foci formation 
after DNA damage. Thus, we propose that FancD2 promotes a subpathway of HR that 
normally mediates gene conversion by a mechanism that avoids crossing over and 
hence SCEs.