Abstract
Broken chromosomes can be repaired by several homologous recombination mechanisms, including gene conversion and break-induced replication (BIR). In
Saccharomyces cerevisiae
, an HO endonuclease-induced double-strand break (DSB) is normally repaired by gene conversion. Previously, we have shown that in the absence of
RAD52
, repair is nearly absent and diploid cells lose the broken chromosome; however, in cells lacking
RAD51
, gene conversion is absent but cells can repair the DSB by BIR. We now report that gene conversion is also abolished when
RAD54, RAD55
, and
RAD57
are deleted but BIR occurs, as with
rad51
Δ cells. DSB-induced gene conversion is not significantly affected when
RAD50, RAD59, TID1
(
RDH54
),
SRS2
, or
SGS1
is deleted. Various double mutations largely eliminate both gene conversion and BIR, including
rad51Δ rad50Δ, rad51Δ rad59
Δ, and
rad54Δ tid1
Δ. These results demonstrate that there is a
RAD51
- and
RAD54
-independent BIR pathway that requires
RAD59, TID1, RAD50
, and presumably
MRE11
and
XRS2
. The similar genetic requirements for BIR and telomere maintenance in the absence of telomerase also suggest that these two processes proceed by similar mechanisms.