Mitotic cyclins regulate telomeric recombination in telomerase-deficient XXXX cells.

@entity20495 @entity42182 @entity11023 @entity42183 @entity12248 @entity11869 @entity375
Telomerase-deficient mutants of @entity375 can survive death by senescence by using one of two homologous recombination pathways. The @entity11023 pathway amplifies the subtelomeric Y' sequences, while the @entity12248 pathway amplifies the telomeric TG(1-3) repeats. Here we show that telomerase-negative cells require @entity20495 (the major B-type cyclin in this organism), in association with @entity11869 ( @entity11869 ), to generate postsenescence survivors at a normal rate. The @entity12248 pathway was more sensitive to the absence of @entity20495 than the @entity11023 pathway. We also report that telomerase @entity12248 @entity11023 triple mutants still generated postsenescence survivors. This novel @entity12248 - and @entity11023 -independent pathway of telomeric recombination also appeared to be controlled by @entity20495 . In telomerase-positive cells, a synthetic growth defect between mutations in @entity20495 and @entity12248 or in its partners in the conserved MRX complex, @entity42182 and @entity42183 , was observed. This genetic interaction was independent of @entity42182 nuclease activity but was dependent on a DNA repair function. The present data reveal an unexpected role of @entity11869 / @entity20495 in telomeric recombination during telomerase-independent maintenance of telomeres. They also uncover a functional interaction between @entity11869 / @entity20495 and MRX during the control of the mitotic cell cycle.
