Send to

Choose Destination
See comment in PubMed Commons below
Chromosoma. 2003 Apr;111(7):429-37. Epub 2003 Mar 11.

Loss of cap structure causes mitotic defect in Tetrahymena thermophila telomerase mutants.

Author information

Department of Biology, Lake Forest College, IL 60045, USA.


Mutation of the telomeric repeat sequence has severe cellular consequences in a variety of systems. A Tetrahymena thermophila telomerase template mutant, ter1-43AA, displays an acute mitotic chromosome segregation defect. In the study described here we investigated the molecular basis for this lethality. Although cloned ter1-43AA macronuclear telomeres had long tracts of wild-type G4T2 repeats, they were capped by a mixture of G4T3 repeats, shown previously to be non-lethal, and G4T4 repeats, the telomeric sequence normally found in hypotrichous ciliates such as Oxytricha. To test further the functionality of the G4T4 repeat sequence in T. thermophila, we devised a new template mutation, ter1-44+AA, that resulted in more uniform synthesis of this sequence at telomere caps in vivo. The ter1-44+AA mutant displayed the most severe mitotic defect reported to date, with up to 85% of the population having micronuclei in anaphase, providing firm evidence that the hypotrich repeat sequence is not functional in Tetrahymena. Surprisingly, in spite of the telomeric sequence mutation, neither the ter1-43AA nor ter1-44+AA mutant displayed any significant loss of telomere length regulation. These results demonstrate that loss of telomere cap integrity, rather than length regulation, leads to the anaphase defect.

[Indexed for MEDLINE]
PubMed Commons home

PubMed Commons

How to join PubMed Commons

    Supplemental Content

    Full text links

    Icon for Springer
    Loading ...
    Support Center