Affiliation:
1. Molecular Cell Biology Laboratory, Graduate School of Pharmaceutical Sciences, Tohoku University, Sendai 980-8578
2. Cell Biology Laboratory, School of Pharmaceutical Sciences, Kinki University, Osaka 577-8502
3. Department of Medical Genetics (Radiation Biology) B4, Graduate School of Medicine, Osaka University, Osaka 565-0871, Japan
Abstract
ABSTRACT
Human
RECQL1
and
RECQL5
belong to the RecQ family that includes Bloom syndrome, Werner syndrome, and Rothmund-Thomson syndrome causative genes. Cells derived from individuals suffering from these syndromes show significant levels of genomic instability. However, neither
RECQL1
nor
RECQL5
has been related to a disease, and nothing is known about the functions of RecQL1 and RecQL5. We generated here
RECQL1
−/−
,
RECQL5
−/−
,
RECQL1
−/−
/RECQL5
−/−
,
RECQL1
−/−
/BLM
−/−
, and
RECQL5
−/−
/BLM
−/−
cells from chicken B-lymphocyte line DT40 cells. Although
BLM
−/−
DT40 cells showed a slow-growth phenotype, a higher sensitivity to methyl methanesulfonate than the wild type, and an ∼10-fold increase in the frequency of sister chromatid exchange (SCE) compared to wild-type cells,
RECQL1
−/−
,
RECQL5
−/−
, and
RECQL1
−/−
/RECQL5
−/−
cells showed no significant difference from the wild-type cells in growth, sensitivity to DNA-damaging agents, and the frequency of SCE. However, both
RECQL1
−/−
/BLM
−/−
and
RECQL5
−/−
/BLM
−/−
cells grew more slowly than
BLM
−/−
cells because of the increase in the population of dead cells, indicating that RecQL1 and RecQL5 are somehow involved in cell viability under the BLM function-impaired condition. Surprisingly,
RECQL5
−/−
/BLM
−/−
cells showed a higher frequency of SCE than
BLM
−/−
cells, indicating that RecQL5 suppresses SCE under the BLM function-impaired condition.
Publisher
American Society for Microbiology
Subject
Cell Biology,Molecular Biology
Cited by
80 articles.
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