To measure the impact of the RAD51 pathway on Sister-Chromatid Exchanges (S
CE), we used hamster cells expressing either the wild-type MmRAD51, which s
timulates, or the dominant negative SMRAD51, which inhibits, gene conversio
n without affecting cell viability of untreated as well as T-rays irradiate
d cells. We show that MmRAD51 did not affect the rate of spontaneous SCE wh
ile it strongly stimulated spontaneous recombination between tandem repeats
. No spontaneous recombinant was detected when expressing SMRAD51 while spo
ntaneous SCE were only slightly diminished. After treatment by an alkylatin
g agent (MNU), MmRAD51 stimulated MNU-induced recombination whereas no reco
mbinant was detected when expressing SMRAD51. MNU induced SCE in all cell l
ines, even in the SMRAD51 expressing lines, but the induction of SCE was sl
ightly more efficient in lines expressing MmRAD51 and less efficient in lin
es expressing SMRAD51. Thus, in mammalian cells, the RAD51-dependent gene c
onversion pathway drastically affects recombination between intrachromosoma
l tandem repeats, whereas it only partially participates in SCE formation,
measured at a chromosomal level. These results show that RAD51-gene convers
ion can participate in induced SCE but that alternative pathways should exi
st.