| Summary: | The regulation of telomere length has a significant impact on cancer risk and aging in humans. Circular chromosomes are found in humans and are often unstable during mitosis, resulting in genome instability. Some types of cancer have a high frequency of a circular chromosome. Fission yeast is a good model for studying the formation and stability of circular chromosomes as deletion of <i>pot1</i> (encoding a telomere protection protein) results in rapid telomere degradation and chromosome fusion. Pot1 binds to single-stranded telomere DNA and is conserved from fission yeast to humans. Loss of <i>pot1</i> leads to viable strains in which all three fission yeast chromosomes become circular. In this review, I will introduce <i>pot1</i> genetic interactions as these inform on processes such as the degradation of uncapped telomeres, chromosome fusion, and maintenance of circular chromosomes. Therefore, exploring genes that genetically interact with <i>pot1</i> contributes to finding new genes and/or new functions of genes related to the maintenance of telomeres and/or circular chromosomes.
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