CHECKPOINT CONTROL ON MITOCHONDRIAL DIVISION IN CYANIDIOSCHYZON MEROLAE

Citation
R. Itoh et al., CHECKPOINT CONTROL ON MITOCHONDRIAL DIVISION IN CYANIDIOSCHYZON MEROLAE, Protoplasma, 196(3-4), 1997, pp. 135-141
Citations number
19
Categorie Soggetti
Cell Biology
Journal title
ISSN journal
0033183X
Volume
196
Issue
3-4
Year of publication
1997
Pages
135 - 141
Database
ISI
SICI code
0033-183X(1997)196:3-4<135:CCOMDI>2.0.ZU;2-V
Abstract
It is generally accepted that mitochondria proliferate by division. Ho wever, since the apparatus for mitochondrial division was discovered o nly recently, the basic mechanism of mitochondrial division remains po orly understood. The unicellular red alga Cyanidioschyzon merolae is t he only organism in which the existence of the apparatus for mitochond rial division (mitochondrion-dividing ring) has been proved by electro n microscopy. Since mitochondrial division, mitosis, and cytokinesis r egularly occurred in that order, we can assume that tight linkage exis ts between mitochondrial division and the mitotic cycle. To examine th is assumption, we performed experiments with aphidicolin, a specific i nhibitor of DNA polymerase a, using cells that had been synchronized b y a 12 h light/12 h dark treatment. The effects of aphidicolin on C. m erolae cells were examined by both epifluorescence and electron micros copy. When cells synchronized at the S phase were treated with aphidic olin, neither mitosis nor cytokinesis occurred. Epifluorescence micros copy after staining with 3,3'-dihexyloxacarbocyanine iodide (DiOC(6); a mitochondrion-specific fluorochrome) revealed that mitochondrial div ision was also completely inhibited. Nevertheless, electronmicroscopic examination of the aphidicolin-treated cells clearly revealed the pre sence of a mitochondrion-dividing ring in mitochondria in all cells ex amined, in spite of the absence of mitochondrial division. Microbodies , which might be related to mitochondrial division in C. merolae, also failed to divide and became attached to the mitochondrion-dividing ri ngs. These results imply the presence of a checkpoint control mechanis m that inhibits division of mitochondria and microbodies in the absenc e of the synthesis of cell-nuclear DNA.