A novel C 1-3 A direct repeat
recombination assay has been established to measure telomeric
recombination. Direct repeat recombination between C 1-3 A
direct repeats is blocked near telomeres. In contrast recombination
between control substrates, direct repeats of either
C 4 A 2 or a unique sequence, is not affected by
telomere proximity. The inhibition is not under the same control as
telomere position effect (TPE) as it is both sequence specific and
mutations in genes essential for TPE do not alleviate the telomeric
repression on recombination. The C 1-3 A specific repression is
eliminated in cells that over express the telomere binding protein,
Rap1, a condition that also increases recombination between yeast
telomeric direct repeats at internal positions on the chromosome. We
propose that the repression of C 1-3 A direct repeat
recombination occurs through the action of a telomere specific end-binding protein. We have used the direct repeat assay in a mutant
screen to look for mutations that specifically increase C 1-3 A
direct repeat recombination. Mutagenesis was performed and ~6000
colonies were screened for hyper-recombination. We identified 6
t elomere h yper- r ecombination ( thr ) mutants
that show increased C 1-3 A direct repeat recombination.
Fluctuation analysis determined that the rates of recombination of the
thr mutants varied from 6-75-fold over wild type rates of
recombination. Preliminary data suggest that the effect on recombination
is specific to C 1-3 A direct repeats. At least one of the
thr mutants shows a telomere length phenotype. Further
characterization and cloning of the thr mutants will provide
insight into the role of recombination in telomere metabolism.
Return to YGM 1998 Abstract Index