Protection of telomere (Pot1) is a single-stranded telomere binding protein which is essential for chromosome ends protection. Fission yeast Rqh1 is a member of RecQ helicases family which has essential roles in the maintenance of genomic stability and regulation of homologous recombination. Double mutant between fission yeast pot1 Delta and rqh1 helicase dead (rqh1-hd) maintains telomere by homologous recombination. In pot1 Delta rqh1-hd double mutant, recombination intermediates accumulate near telomere which disturb chromosome segregation and make cells sensitive to microtubule inhibitors thiabendazole (TBZ). Deletion of chk1(+) or mutation of its kinase domain shortens the G2 of pot1 Delta rqh-1d double mutant and suppresses both the accumulation of recombination intermediates and the TBZ sensitivity of that double mutant. In this study, we asked whether the long G2 is the reason for the TBZ sensitivity of pot1 Delta rqh1-hd double mutant. We found that shortening the G2 of pot1 Delta rqh1-hd double mutant by additional mutations of wee1 and mik1 or gain of function mutation of Cdc2 suppresses both the accumulation of recombination intermediates and the TBZ sensitivity of pot1 Delta rqh1-hd double mutant. Our results suggest that long G2 of pot1 Delta rqh1-hd double mutant may allow time for the accumulation of recombination intermediates which disturb chromosome segregation and make cells sensitive to TBZ. (C) 2015 Elsevier Inc. All rights reserved.