Yeast cells lacking a functional EST1 gene show progressive shortening
of the terminal G1-3T telomeric repeats and a parallel increase in th
e frequency of cell death. Although the majority of the cells in an es
t1-culture die, a minor subpopulation survives the potentially lethal
consequences of the est1 mutation. We show that these est1- survivors
arise as a result of the amplification and acquisition of subtelomeric
elements (and their deletion derivatives) by a large number of telome
res. Hence, even when the primary pathway for telomere replication is
defective, an alternative backup pathway can restore telomere function
and keep the cell alive.