Interaction of ATP17 gene with SUP45 and SUP35 genes in Saccharomyces cerevisiae yeast

Genes SUP35 and SUP45 have been identified in the saccharomycete yeast as genes controlling termination of translation in cytoplasmic ribosomes. However, many facts indicate that the control of translation termination is not the only function of these genes. This work is devoted to studying one of the pleiotropic effects of sup35 and sup45 mutations, a respiratory deficiency. The compensation for this deficiency in mutants for either gene can occur due to a mutation in the ATP17 gene encoding the f-subunit of mitochondrial F1F0 ATP synthase. It is assumed that the observed interaction can be related to the system of co-translational protein import into mitochondria.     

Inhibition of 2,4-dinitrophenol-induced potassium efflux by adenine nucleotides in mitochondria

The influence of nucleotides on 2,4-dinitrophenol (DNP)-induced K+ efflux from intact rat liver mitochondria has been studied. ATP and ADP at micromolar concentrations were found to inhibit mitochondrial potassium transport, whereas GTP, GDP, CTP, and UTP did not show tha same effect. The values of half-maximal inhibition (IC50) were approximately 20 microM for ATP and approximately 60 microM for ADP. It is suggested that adenine nucleotides exert their inhibitory action at the matrix side of the inner mitochondrial membrane since the inhibitor of adenine nucleotide translocase atractyloside at concentration of 1 microM completely removed the inhibitory effect of ATP and ADP. The mitochondrial ATPase inhibitor oligomycin (2 microg/ml) was found to reduce slightly the rate of DNP-induced K+ efflux and had no effect on inhibition by adenine nucleotides; the latter was insensitive to Mg2+ and the changes in pH. It seems likely that the regulation of potassium transport is not due to phosphorylation of the channel-forming protein but to binding of the nucleotides in specific regulatory sites. The possibility of potassium efflux from mitochondria in the presence of uncoupler via the ATP-dependent potassium channel is discussed.     

Central pool of serotonin and tail-flick latency during two phases of biphasic fever in rats

In experiments on male Wistar rats, the acute phase reaction was induced by a bolus intravenous injection of Escherichia coli lipopolysaccharide (10 microg/kg) through a silicon catheter pre-implanted into the jugular vein. The colonic and skin temperature was measured with thermocouples. Changes in nociception were assessed based on tail flick latency (TFL) in response to a noxious heat stimulus. In this work, we observed the development of biphasic fever and phasic changes in TFL, namely, hyperalgesia in the first period of the acute phase reaction and hypoalgesia in its second phase. The catabolism of serotonin increased most considerably in the initial period of the acute phase reaction in the midbrain, striatum, and rostrodorsomedial medulla (on average, by 20-25%, 35-40%, and 95-100%, respectively). In the second phase of the acute phase reaction, despite a significant increase in the serotonin content in the striatum, midbrain, and cerebellum, there were no significant changes in serotonin catabolism in these parts of the CNS, which coincided with hypoalgesia. Thus, the phasic changes in TFL and colonic temperature after initiation of the acute phase reaction were accompanied by determinate changes in the catabolism of serotonin in different brain parts.