An alternative pathway for yeast telomere maintenance rescues est1- senescence.
Yeast cells lacking a functional EST1 gene show progressive shortening of the terminal G1-3T telomeric repeats and a parallel increase in the frequency of cell death. Although the majority of the cells in an est1- 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 telomeres. Hence, even when the primary pathway for telomere replication is defective, an alternative backup pathway can restore telomere function and keep the cell alive.
Lundblad
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Department of Microbiology and Immunology University of California, San Francisco 94143-0414.
Blackburn
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EH
D001483:Base Sequence; D003001:Cloning, Molecular; D004261:DNA Replication; D004271:DNA, Fungal / Q000235:genetics; D005656:Fungal Proteins / Q000235:genetics*; D005800:Genes, Fungal; D008969:Molecular Sequence Data; D009838:Oligodeoxyribonucleotides / Q000737:chemistry; D011995:Recombination, Genetic; D012091:Repetitive Sequences, Nucleic Acid; D015183:Restriction Mapping; D012441:Saccharomyces cerevisiae / Q000235:genetics*; D016615:Telomere
D004271:DNA, Fungal; D005656:Fungal Proteins; D009838:Oligodeoxyribonucleotides