The Telomere and Telomerase: How do they Interact?

  1. Derek J. Chadwick Organizer and
  2. Gail Cardew Organizer
  1. E. Blackburn,
  2. A. Bhattacharyya,
  3. D. Gilley,
  4. K. Kirk,
  5. A. Krauskopf,
  6. M. McEachern,
  7. J. Prescott and
  8. T. Ware

Published Online: 28 SEP 2007

DOI: 10.1002/9780470515433.ch2

Ciba Foundation Symposium 211 - Telomeres and Telomerase

Ciba Foundation Symposium 211 - Telomeres and Telomerase

How to Cite

Blackburn, E., Bhattacharyya, A., Gilley, D., Kirk, K., Krauskopf, A., McEachern, M., Prescott, J. and Ware, T. (2007) The Telomere and Telomerase: How do they Interact?, in Ciba Foundation Symposium 211 - Telomeres and Telomerase (eds D. J. Chadwick and G. Cardew), John Wiley & Sons, Ltd., Chichester, UK. doi: 10.1002/9780470515433.ch2

Author Information

  1. Departments of Microbiology and Immunology, and of Biochemistry and Biophysics, University of California, San Francisco, CA 94143-0414, USA

Publication History

  1. Published Online: 28 SEP 2007

ISBN Information

Print ISBN: 9780471972785

Online ISBN: 9780470515433



  • telomere length homeostasis;
  • telomerase rna mutations;
  • linear eukaryotic chromosomes;
  • mutating telomeric DNA;
  • telomerase enzymatic action


The tandemly repeated DNA sequence of telomeres is typically specified by the ribonucleoprotein enzyme telomerase. Telomerase copies part of its intrinsic RNA moiety to make one strand of the telomeric repeat DNA. Recent work has led to the concept of a telomere homeostasis system. We have been studying two key physical components of this system: the telomere itself and telomerase. Mutating the template sequence of telomerase RNA caused various phenotypes: (1) mutating specific residues in the ciliate Tetrabymena and two yeasts showed that they are required for critical aspects of telomerase action; (2) certain mutated telomeric sequences caused a previously unreported phenotype, i.e. a strong anaphase block in Tetrabymena micronuclei; and (3) certain template mutations in the telomerase RNA gene of the yeast Kluyveromyceslactis led to unregulated telomere elongation, which in some cases was directly related to loss of binding to K. lactis Raplp. Using K. lactis carrying alterations in the genes for Raplp and other silencing components, we proposed a general model for telomere length homeostasis: namely, that the structure and DNA length of the DNA–protein complex that comprises the telomere are key determinants of telomerase access, and hence the frequency of action of telomerase, at the telomere.