The molecular function of mTERFs (mitochondrial
transcription termination factors) has so far only
been described for metazoan members of the
protein family and in animals they control mitochondrial
replication, transcription and translation. Cells of
photosynthetic eukaryotes harbour chloroplasts and
mitochondria, which are in an intense cross-talk that
is vital for photosynthesis. Chlamydomonas
reinhardtii is a unicellular green alga widely used as
a model organism for photosynthesis research and
green biotechnology. Among the six nuclear C.
reinhardtii mTERF genes is mTERF-like gene of
Chlamydomonas (MOC1), whose inactivation alters
mitorespiration and interestingly also light-acclimation
processes in the chloroplast that favour the
enhanced production of biohydrogen. We show here
from in vitro studies that MOC1 binds specifically to a
sequence within the mitochondrial rRNA-coding
module S3, and that a knockout of MOC1 in the
mutant stm6 increases read-through transcription at
this site, indicating that MOC1 acts as a transcription
terminator in vivo. Whereas the level of certain
antisense RNA species is higher in stm6, the amount
of unprocessed mitochondrial sense transcripts is
strongly reduced, demonstrating that a loss of MOC1
causes perturbed mitochondrial DNA (mtDNA) expression.
Overall, we provide evidence for the existence
of mitochondrial antisense RNAs in C. reinhardtii
and show that mTERF-mediated transcription termination
is an evolutionary-conserved mechanism
occurring in phototrophic protists and metazoans.