摘要：SummaryMalaria remains a major cause of morbidity and mortality in the developing world. Recent work has implicated chromosome end stability and the repair of DNA breaks through telomere healing as potent drivers of variant antigen diversification, thus associating basic mechanisms for maintaining genome integrity with aspects of host-parasite interactions. Here we applied long-read sequencing technology to precisely examine the dynamics of telomere addition and chromosome end stabilization in response to double-strand breaks within subtelomeric regions. We observed that the process of telomere healing induces the initial synthesis of telomere repeats well in excess of the minimal number required for end stability. However, once stabilized, these newly created telomeres appear to function normally, eventually returning to a length nearing that of intact chromosome ends. These results parallel recent observations in humans, suggesting an evolutionarily conserved mechanism for chromosome end repair.Graphical AbstractDisplay OmittedHighlights•Subtelomeric domains of malaria parasites contain virulence genes•Exposure to DNA damage causes a genome-wide increase in telomere lengths•Broken chromosome ends undergo telomere healing, extending their length•The extended number of repeats at healed telomeres lessens over timeAstrobiology; chromosome organization; omics; parasitology
