PMID- 25030699
OWN - NLM
STAT- MEDLINE
DCOM- 20140905
LR  - 20211021
IS  - 1549-5477 (Electronic)
IS  - 0890-9369 (Print)
IS  - 0890-9369 (Linking)
VI  - 28
IP  - 14
DP  - 2014 Jul 15
TI  - A cell cycle-regulated Slx4-Dpb11 complex promotes the resolution of DNA repair 
      intermediates linked to stalled replication.
PG  - 1604-19
LID - 10.1101/gad.240515.114 [doi]
AB  - A key function of the cellular DNA damage response is to facilitate the bypass of 
      replication fork-stalling DNA lesions. Template switch reactions allow such a 
      bypass and involve the formation of DNA joint molecules (JMs) between sister 
      chromatids. These JMs need to be resolved before cell division; however, the 
      regulation of this process is only poorly understood. Here, we identify a 
      regulatory mechanism in yeast that critically controls JM resolution by the 
      Mus81-Mms4 endonuclease. Central to this regulation is a conserved complex 
      comprising the scaffold proteins Dpb11 and Slx4 that is under stringent control. 
      Cell cycle-dependent phosphorylation of Slx4 by Cdk1 promotes the Dpb11-Slx4 
      interaction, while in mitosis, phosphorylation of Mms4 by Polo-like kinase Cdc5 
      promotes the additional association of Mus81-Mms4 with the complex, thereby 
      promoting JM resolution. Finally, the DNA damage checkpoint counteracts 
      Mus81-Mms4 binding to the Dpb11-Slx4 complex. Thus, Dpb11-Slx4 integrates several 
      cellular inputs and participates in the temporal program for activation of the 
      JM-resolving nuclease Mus81.
CI  - (c) 2014 Gritenaite et al.; Published by Cold Spring Harbor Laboratory Press.
FAU - Gritenaite, Dalia
AU  - Gritenaite D
AD  - DNA Replication and Genome Integrity, Max-Planck Institute of Biochemistry, 82152 
      Martinsried, Germany;
FAU - Princz, Lissa N
AU  - Princz LN
AD  - DNA Replication and Genome Integrity, Max-Planck Institute of Biochemistry, 82152 
      Martinsried, Germany;
FAU - Szakal, Barnabas
AU  - Szakal B
AD  - Fondazione IFOM, Istituto FIRC di Oncologia Molecolare, 20139 Milan, Italy;
FAU - Bantele, Susanne C S
AU  - Bantele SC
AD  - DNA Replication and Genome Integrity, Max-Planck Institute of Biochemistry, 82152 
      Martinsried, Germany;
FAU - Wendeler, Lina
AU  - Wendeler L
AD  - DNA Replication and Genome Integrity, Max-Planck Institute of Biochemistry, 82152 
      Martinsried, Germany;
FAU - Schilbach, Sandra
AU  - Schilbach S
AD  - DNA Replication and Genome Integrity, Max-Planck Institute of Biochemistry, 82152 
      Martinsried, Germany;
FAU - Habermann, Bianca H
AU  - Habermann BH
AD  - Computational Biology, Max-Planck Institute of Biochemistry, 82152 Martinsried, 
      Germany;
FAU - Matos, Joao
AU  - Matos J
AD  - Institute of Biochemistry, Eidgenossische Technische Hochschule Zurich, 8093 
      Zurich, Switzerland;
FAU - Lisby, Michael
AU  - Lisby M
AD  - Department of Biology, University of Copenhagen, 2200 Copenhagen, Denmark.
FAU - Branzei, Dana
AU  - Branzei D
AD  - Fondazione IFOM, Istituto FIRC di Oncologia Molecolare, 20139 Milan, Italy;
FAU - Pfander, Boris
AU  - Pfander B
AD  - DNA Replication and Genome Integrity, Max-Planck Institute of Biochemistry, 82152 
      Martinsried, Germany;
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - Genes Dev
JT  - Genes & development
JID - 8711660
RN  - 0 (Cell Cycle Proteins)
RN  - 0 (DPB11 protein, S cerevisiae)
RN  - 0 (Saccharomyces cerevisiae Proteins)
RN  - EC 3.1.- (Endodeoxyribonucleases)
RN  - EC 3.1.- (SLX4 protein, S cerevisiae)
SB  - IM
MH  - Cell Cycle
MH  - Cell Cycle Proteins/*metabolism
MH  - DNA Repair/*physiology
MH  - *DNA Replication
MH  - Endodeoxyribonucleases/genetics/*metabolism
MH  - Enzyme Activation/physiology
MH  - Mutation/genetics
MH  - Phosphorylation
MH  - Protein Binding
MH  - Saccharomyces cerevisiae/enzymology/genetics/*metabolism
MH  - Saccharomyces cerevisiae Proteins/genetics/*metabolism
PMC - PMC4102767
OTO - NOTNLM
OT  - DNA damage response
OT  - cell cycle
OT  - homologous recombination
OT  - joint molecule resolution
OT  - post-replicative repair
EDAT- 2014/07/18 06:00
MHDA- 2014/09/06 06:00
PMCR- 2015/01/15
CRDT- 2014/07/18 06:00
PHST- 2014/07/18 06:00 [entrez]
PHST- 2014/07/18 06:00 [pubmed]
PHST- 2014/09/06 06:00 [medline]
PHST- 2015/01/15 00:00 [pmc-release]
AID - 28/14/1604 [pii]
AID - 10.1101/gad.240515.114 [doi]
PST - ppublish
SO  - Genes Dev. 2014 Jul 15;28(14):1604-19. doi: 10.1101/gad.240515.114.