Functional Relation among RecQ Family Helicases RecQL1, RecQL5, and BLM in Cell Growth and Sister Chromatid Exchange Formation

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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.