Eukaryotic Cell doi:10.1128/EC.00393-07
Copyright (c) 2008, American Society for Microbiology and/or the Listed Authors/Institutions. All Rights Reserved.
Abnormal micronuclear telomeres lead to an unusual cell cycle checkpoint and defects in Tetrahymena oral morphogenesis
Karen E. Kirk*,
Christina Christ,
Jennifer M. McGuire,
Arun G. Paul,
Mithaq Vahedi,
Kathleen R. Stuart,
and
Eric S. Cole
Department of Biology, Lake Forest College, Lake Forest, IL 60045; Department of Biology, St. Olaf College, Northfield MN 55057
* To whom correspondence should be addressed. Email:
kirk{at}lakeforest.edu.
 |
Abstract |
|---|
Telomere mutants have been well studied with respect to telomerase and the role of telomere binding proteins, but they have not been used to explore how a downstream morphogenic event is related to the mutated telomeric DNA. We report that alterations at the telomeres can have profound consequences on organellar morphogenesis. Specifically, a telomerase RNA mutation termed ter1-43AA results in the loss of germline micronuclear telomeres in the binucleate protozoan, Tetrahymena thermophila. These cells also display a micronuclear mitotic arrest, characterized by an extreme delay in anaphase with elongated condensed chromatin and a mitotic spindle apparatus. This anaphase defect suggests telomere fusions, and consequently a spindle rather than a DNA damage checkpoint. Most surprisingly, these mutants exhibit unique, dramatic defects in the formation of the cell's oral apparatus. We suggest that micronuclear telomere loss leads to a "dynamic pause" in the program of cortical development, which may reveal an unusual cell cycle checkpoint.
Previous Article | Next Article 
