PMID- 30453647
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20191120
IS  - 2073-4425 (Print)
IS  - 2073-4425 (Electronic)
IS  - 2073-4425 (Linking)
VI  - 9
IP  - 11
DP  - 2018 Nov 17
TI  - Fanconi Anaemia-Like Mph1 Helicase Backs up Rad54 and Rad5 to Circumvent 
      Replication Stress-Driven Chromosome Bridges.
LID - 10.3390/genes9110558 [doi]
LID - 558
AB  - Homologous recombination (HR) is a preferred mechanism to deal with DNA 
      replication impairments. However, HR synapsis gives rise to joint molecules (JMs) 
      between the nascent sister chromatids, challenging chromosome segregation in 
      anaphase. Joint molecules are resolved by the actions of several 
      structure-selective endonucleases (SSEs), helicases and topoisomerases. 
      Previously, we showed that yeast double mutants for the Mus81-Mms4 and Yen1 SSEs 
      lead to anaphase bridges (ABs) after replication stress. Here, we have studied 
      the role of the Mph1 helicase in preventing these anaphase aberrations. Mph1, the 
      yeast ortholog of Fanconi anaemia protein M (FANCM), is involved in the removal 
      of the D-loop, the first JM to arise in canonical HR. Surprisingly, the absence 
      of Mph1 alone did not increase ABs; rather, it blocked cells in G2. 
      Interestingly, in the search for genetic interactions with functionally related 
      helicases and translocases, we found additive effects on the G2 block and post-G2 
      aberrations between mph1Delta and knockout mutants for Srs2, Rad54 and Rad5. Based on 
      these interactions, we suggest that Mph1 acts coordinately with these helicases 
      in the non-canonical HR-driven fork regression mechanism to bypass stalled 
      replication forks.
FAU - Garcia-Luis, Jonay
AU  - Garcia-Luis J
AD  - Unidad de Investigacion, Hospital Universitario Nuestra Senora de Candelaria, 
      Carretera del Rosario, 145, 38010 Santa Cruz de Tenerife, Spain. 
      j.garcia-luis@lms.mrc.ac.uk.
FAU - Machin, Felix
AU  - Machin F
AUID- ORCID: 0000-0003-4559-7798
AD  - Unidad de Investigacion, Hospital Universitario Nuestra Senora de Candelaria, 
      Carretera del Rosario, 145, 38010 Santa Cruz de Tenerife, Spain. 
      fmachin@funcanis.es.
AD  - Instituto de Tecnologias Biomedicas, Universidad de La Laguna, C/Sta Maria 
      Soledad, 38200 San Cristobal de La Laguna, Santa Cruz de Tenerife, Spain. 
      fmachin@funcanis.es.
LA  - eng
GR  - BFU2015-63902-R/Ministerio de Economia, Industria y Competitividad, Gobierno de 
      Espana/
GR  - BFU2017-83954-R/Ministerio de Economia, Industria y Competitividad, Gobierno de 
      Espana/
GR  - AP2009-2511/Ministerio de Educacion, Cultura y Deporte/
PT  - Journal Article
DEP - 20181117
PL  - Switzerland
TA  - Genes (Basel)
JT  - Genes
JID - 101551097
PMC - PMC6266064
OTO - NOTNLM
OT  - G2 arrest
OT  - Mph1 (FANCM)
OT  - Rad5 (HTLF)
OT  - Rad54
OT  - Sgs1 (BLM)
OT  - Srs2
OT  - anaphase bridges
OT  - fork regression
OT  - methyl methanesulfonate
OT  - replication stress
COIS- The authors declare no conflict of interest.
EDAT- 2018/11/21 06:00
MHDA- 2018/11/21 06:01
PMCR- 2018/11/01
CRDT- 2018/11/21 06:00
PHST- 2018/10/25 00:00 [received]
PHST- 2018/11/13 00:00 [revised]
PHST- 2018/11/13 00:00 [accepted]
PHST- 2018/11/21 06:00 [entrez]
PHST- 2018/11/21 06:00 [pubmed]
PHST- 2018/11/21 06:01 [medline]
PHST- 2018/11/01 00:00 [pmc-release]
AID - genes9110558 [pii]
AID - genes-09-00558 [pii]
AID - 10.3390/genes9110558 [doi]
PST - epublish
SO  - Genes (Basel). 2018 Nov 17;9(11):558. doi: 10.3390/genes9110558.