Format

Send to

Choose Destination
See comment in PubMed Commons below
Mol Microbiol. 2008 Dec;70(6):1465-76. doi: 10.1111/j.1365-2958.2008.06493.x. Epub 2008 Oct 22.

A new function of Trypanosoma brucei mitochondrial topoisomerase II is to maintain kinetoplast DNA network topology.

Author information

1
Department of Biological Chemistry, Johns Hopkins Medical School, Baltimore, MD, USA.

Abstract

The mitochondrial genome of Trypanosoma brucei, called kinetoplast DNA, is a network of topologically interlocked DNA rings including several thousand minicircles and a few dozen maxicircles. Kinetoplast DNA synthesis involves release of minicircles from the network, replication of the free minicircles and reattachment of the progeny. Here we report a new function of the mitochondrial topoisomerase II (TbTOP2mt). Although traditionally thought to reattach minicircle progeny to the network, here we show that it also mends holes in the network created by minicircle release. Network holes are not observed in wild-type cells, implying that this mending reaction is normally efficient. However, RNAi of TbTOP2mt causes holes to persist and enlarge, leading to network fragmentation. Remarkably, these network fragments remain associated within the mitochondrion, and many appear to be appropriately packed at the local level, even as the overall kinetoplast organization is dramatically altered. The deficiency in mending holes is temporally the earliest observable defect in the complex TbTOP2mt RNAi phenotype.

PMID:
19019151
PMCID:
PMC2993328
DOI:
10.1111/j.1365-2958.2008.06493.x
[Indexed for MEDLINE]
Free PMC Article
PubMed Commons home

PubMed Commons

0 comments
How to join PubMed Commons

    Supplemental Content

    Full text links

    Icon for Wiley Icon for PubMed Central
    Loading ...
    Support Center