87 research outputs found
MTERF factors: a multifunction protein family
The MTERF family is a large protein family, identified in
metazoans and plants, which consists of four subfamilies,
MTERF1, 2, 3 and 4. Mitochondrial localisation was predicted
for the vast majority of MTERF family members and
demonstrated for the characterised MTERF proteins. The
main structural feature of MTERF proteins is the presence
of a modular architecture, based on repetitions of a 30-residue
module, the mTERF motif, containing leucine zipperlike
heptads. The MTERF family includes transcription
termination factors: human mTERF, sea urchin mtDBP and
Drosophila DmTTF. In addition to terminating transcription,
they are involved in transcription initiation and in the control
of mtDNA replication. This multiplicity of functions seems
to flank differences in the gene organisation of mitochondrial
genomes. MTERF2 and MTERF3 play antithetical roles in
controlling mitochondrial transcription: that is, mammalian
and Drosophila MTERF3 act as negative regulators, whereas
mammalian MTERF2 functions as a positive regulator. Both
proteins contact mtDNA in the promoter region, perhaps
establishing interactions, either mutual or with other factors.
Regulation of MTERF gene expression in human and Drosophila
depends on nuclear transcription factors NRF-2 and
DREF, respectively, and proceeds through pathways which
appear to discriminate between factors positively or negatively
acting in mitochondrial transcription. In this emerging
scenario, it appears that MTERF proteins act to coordinate
mitochondrial transcription
Decrease of D-loop frequency in heart and cerebral hemispheres mitochondrial DNA of aged rat
A quantitative analysis of the frequency of the supercoiled mitochondrial DNA molecules containing the D-loop in rat heart and cerebral hemispheres, at different ages, is presented. Both tissues of aged animals exhibit a remarkable reduction in the content of supercoiled D-loop containing molecules compared to the adults. This alteration could be responsible for the age-dependent reduction of mitochondrial DNA transcription previously observed in rat brain and heart
LIPID-COMPOSITION IN SYNAPTIC AND NONSYNAPTIC MITOCHONDRIA FROM RAT BRAINS AND EFFECT OF AGING
The cholesterol, phospholipid, and fatty acid compositions in synaptic and nonsynaptic mitochondria from rat brains and the effect of aging were studied. Both cholesterol and phospholipid contents were found to be significantly different in synaptic compared to nonsynaptic mitochondria. In both types of brain mitochondria, aging decreases the cholesterol content by 27% and the phospholipid content by approximately 12%. The difference between these decreases observed in the organelles causes decreases in the cholesterol/phospholipid molar ratios for synaptic and nonsynaptic mitochondria of 17 and 19%, respectively. Also, the phospholipid composition is significantly different in synaptic compared to nonsynaptic mitochondria. Among phospholipids, only the cardiolipin fraction showed a significant decrease (26%) in nonsynaptic mitochondria from the brains of aged rats. Instead, the fatty acid composition was not significantly different in synaptic compared to nonsynaptic mitochondria. The 21% aging decrease in linoleic acid (18:2), observed only in nonsynaptic mitochondria, may be related to a decrease in cardiolipin, which contains a large amount of this fatty acid
ACETYL-L-CARNITINE INCREASES CYTOCHROME-OXIDASE SUBUNIT-I MESSENGER-RNA CONTENT IN HYPOTHYROID RAT-LIVER
The effect of acetyl-L-carnitine on the quantity of the messenger RNA for the subunit I of cytochrome oxidase in the liver mitochondria of hypothyroid rat was measured by Northern blot and solution hybridization. Three hours after pre-treatment of hypothyroid rat with acetyl-L-carnitine, the level of the transcript increased strongly. This effect was also obtained when acetyl-L-carnitine was administered to T3 pre-treated hypothyroid rats. These results add further evidence to the suggestion that acetyl-L-carnitine is able to stimulate mitochondrial transcription under altered metabolic conditions
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