Telomerase lost?

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• 作者：James M. Mason ; Thomas A. Randall ; Radmila Capkova Frydrychova
• 刊名：Chromosoma
• 出版年：2016
• 出版时间：March 2016
• 年：2016
• 卷：125
• 期：1
• 页码：65-73
• 全文大小：1,321 KB
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• 作者单位：James M. Mason (1)
  Thomas A. Randall (2)
  Radmila Capkova Frydrychova (3)
  
  1. Laboratory of Genome Integrity and Structural Biology, National Institute of Environmental Health Sciences, Research Triangle Park, NC, USA
  2. Integrative Bioinformatics, National Institute of Environmental Health Sciences, Research Triangle Park, NC, USA
  3. Institute of Entomology, Biology Centre AS CR, Ceske Budejovice, Czech Republic
  
• 刊物类别：Biomedical and Life Sciences
• 刊物主题：Life Sciences
  Cell Biology
  Developmental Biology
  Biochemistry
  Human Genetics
  Animal Genetics and Genomics
  Eukaryotic Microbiology
  
• 出版者：Springer Berlin / Heidelberg
• ISSN：1432-0886

文摘

Telomerase and telomerase-generated telomeric DNA sequences are widespread throughout eukaryotes, yet they are not universal. Neither telomerase nor the simple DNA repeats associated with telomerase have been found in some plant and animal species. Telomerase was likely lost from Diptera before the divergence of Diptera and Siphonaptera, some 260 million years ago. Even so, Diptera is one of the most successful animal orders, making up 11 % of known animal species. In addition, many species of Coleoptera and Hemiptera seem to lack canonical telomeric repeats at their chromosome ends. These and other insects that appear to lack canonical terminal repeat sequences account for another 10–15 % of animal species. Conversely, the silk moth Bombyx mori maintains canonical telomeric sequences at its chromosome ends but seems to lack a functional telomerase. We speculate that a telomere-specific capping complex that recognizes the telomeric repeats and protects chromosome ends is the determining factor in maintaining canonical telomeric sequences and that telomerase is an early and efficacious mechanism for satisfying the needs of capping complex. There are alternate mechanisms for maintaining chromosome ends that do not depend on telomerase, such as recombination found in some human cancer cells and yeast mutants. These mechanisms may maintain the canonical telomeric repeats or allow the terminal sequence to evolve when specificity of the capping complex for terminal repeat sequences is weak.