Telomere is a ribonucleoprotein complex that protects the natural ends of the linear chromosome. Telomere length is mainly maintained by telomerase, a reverse transcriptase that adds telomere repeat sequence. However recombination-dependent mechanism for telomere maintenance also exist in yeast and human cancer cells. In Caenorhabditis elegans, some of telomerase deletion mutant, trt-1(ok410), can maintain the telomere by alternative lengthening of telomeres (ALT). However the molecular mechanism of ALT in worms is largely unknown. In this study, we established stably maintained ALT survivors of worms that activate an ALT mechanism to escape from the sterility phenotype caused by telomerase deletion. By whole genome sequencing and mapping we concluded that mutation may not be required to maintain ALT telomere in these survivors. Interestingly, ALT survivors added either of two specific internal genomic regions as templates for ALT(T-ALT) according to their genetic backgrounds. A T-ALT sequence consists of telomere-like repeat sequence with unrelated sequence in between. T-ALTs had already been copied to a proximal telomere region of the same chromosome prior to ALT activation in nature, and were amplified interchromosomally by ALT activation. Here we propose a hypothesis that the existence of T-ALT structure in the proximal telomere may be one of the prerequisites for ALT activation..
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