Shu proteins promote the formation of homologous recombination intermediates that are processed by Sgs1-Rmi1-Top3
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Shu proteins promote the formation of homologous recombination intermediates that are processed by Sgs1-Rmi1-Top3. / Mankouri, Hocine W; Ngo, Hien-Ping; Hickson, Ian D.
In: Molecular Biology of the Cell, Vol. 18, No. 10, 01.10.2007, p. 4062-73.Research output: Contribution to journal › Journal article › Research › peer-review
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TY - JOUR
T1 - Shu proteins promote the formation of homologous recombination intermediates that are processed by Sgs1-Rmi1-Top3
AU - Mankouri, Hocine W
AU - Ngo, Hien-Ping
AU - Hickson, Ian D
PY - 2007/10/1
Y1 - 2007/10/1
N2 - CSM2, PSY3, SHU1, and SHU2 (collectively referred to as the SHU genes) were identified in Saccharomyces cerevisiae as four genes in the same epistasis group that suppress various sgs1 and top3 mutant phenotypes when mutated. Although the SHU genes have been implicated in homologous recombination repair (HRR), their precise role(s) within this pathway remains poorly understood. Here, we have identified a specific role for the Shu proteins in a Rad51/Rad54-dependent HRR pathway(s) to repair MMS-induced lesions during S-phase. We show that, although mutation of RAD51 or RAD54 prevented the formation of MMS-induced HRR intermediates (X-molecules) arising during replication in sgs1 cells, mutation of SHU genes attenuated the level of these structures. Similar findings were also observed in shu1 cells in which Rmi1 or Top3 function was impaired. We propose a model in which the Shu proteins act in HRR to promote the formation of HRR intermediates that are processed by the Sgs1-Rmi1-Top3 complex.
AB - CSM2, PSY3, SHU1, and SHU2 (collectively referred to as the SHU genes) were identified in Saccharomyces cerevisiae as four genes in the same epistasis group that suppress various sgs1 and top3 mutant phenotypes when mutated. Although the SHU genes have been implicated in homologous recombination repair (HRR), their precise role(s) within this pathway remains poorly understood. Here, we have identified a specific role for the Shu proteins in a Rad51/Rad54-dependent HRR pathway(s) to repair MMS-induced lesions during S-phase. We show that, although mutation of RAD51 or RAD54 prevented the formation of MMS-induced HRR intermediates (X-molecules) arising during replication in sgs1 cells, mutation of SHU genes attenuated the level of these structures. Similar findings were also observed in shu1 cells in which Rmi1 or Top3 function was impaired. We propose a model in which the Shu proteins act in HRR to promote the formation of HRR intermediates that are processed by the Sgs1-Rmi1-Top3 complex.
KW - Cell Proliferation
KW - DNA Repair
KW - DNA-Binding Proteins
KW - Epistasis, Genetic
KW - Genes, Fungal
KW - Hydroxyurea
KW - Methyl Methanesulfonate
KW - Models, Biological
KW - Mutant Proteins
KW - Mutation
KW - RecQ Helicases
KW - Recombination, Genetic
KW - Saccharomyces cerevisiae
KW - Saccharomyces cerevisiae Proteins
U2 - 10.1091/mbc.E07-05-0490
DO - 10.1091/mbc.E07-05-0490
M3 - Journal article
C2 - 17671161
VL - 18
SP - 4062
EP - 4073
JO - Molecular Biology of the Cell
JF - Molecular Biology of the Cell
SN - 1059-1524
IS - 10
ER -
ID: 33752923