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.