PubMed · 2158508
The source did not provide an abstract. Follow the original record for more information.
Explore connections, maps & timelines
J R Tucci. 1990. Hyperthyroidism and pregnancy.. https://doi.org/10.1007/bf03349538
Cite the original work for its findings. Save a collection to share your selection of sources.
KEEP EXPLORING
cAMP represses the transcription of some Saccharomyces cerevisiae genes sensitive to catabolite repression. The effect of cAMP on the expression of FBP1, encoding fructose-1,6-bisphosphatase (FbPase), has been further investigated. In yeast cells shifted to a derepressing medium, synthesis of FbPase was delayed if the strong decrease in intracellular cAMP, which occurs during the shift, was prevented. A similar delay occurred in a RAS2val19 strain, while in a tpk1w strain, with weak protein kinase A activity, induction of FbPase occurred earlier than in a TPK1 strain. In the tpk1w strain, proteins which bind the UAS1 element of FBP1 were present during growth on glucose but they were only weakly operative. Expression of CAT8 and SIP4, encoding proteins which bind the UAS2 element, was blocked by a high concentration of cAMP, but catabolite repression of these genes was not much relieved in a tpk1w strain. We conclude that in S. cerevisiae, as reported for Schizosaccharomyces pombe, control of FBP1 requires both cAMP-dependent and independent pathways; however, the mechanisms operating in the two yeasts are different.
The hypoxic SRP1/TIR1 gene encodes a stress-response cell wall mannoprotein and this gene is downregulated at acidic pH. The stress-responsive HOG pathway is necessary to maintain hypoxic TIR1 expression, but only at acidic pH. However, unlike known HOG pathway-dependent genes, TIR1 is under positive cAMP control and this effect is mediated by GPA2 but not by RAS2. Genetic analysis showed that ord1 mutation was epistatic to the gpa2 mutation, thereby indicating that Gpa2p is needed to counteract the Ord1 factor, which is involved in the repression of hypoxic TIR1 expression, while the HOG pathway appears to be independent from Ord1 repression. In addition, an increased ORD1 gene expression was observed in the Deltagpa2 mutant cells, meaning that GPA2 maintains a low basal level of ORD1 transcripts. Thus, cAMP allows partial relief of the TIR1 repression exerted by Ord1p. However, this is contradicted at acidic pH by the HOG pathway requirement because Hog1p is activated under stress conditions when the cAMP cellular content is low. The opposite effects of the GPA2-cAMP and HOG pathways are likely to explain the diminished hypoxic expression of TIR1 at acidic pH.
Methionine auxotrophs of Ustilago maydis were deficient in mating; unlike wild-type cells, they neither induced nor produced normal mating filaments in the presence of compatible cells. The deficiency was most severe when cells were located some distance apart, but when in direct contact with compatible cells methionine auxotrophs mated and infected plants fairly normally. The mating deficiency was genetically linked to the methionine auxotrophy, segregating with it through in planta crosses. Wild-type cells exposed to the methyltransferase inhibitors ethionine and homocysteine thiolactone were similarly impaired in mating. Exogenous methionine, S-adenosylmethionine (SAM), synthetic mating pheromone, or cAMP all compensated for the mating impairment of the auxotrophs to some extent. Although SAM-dependent methylation could influence activities of various molecules in diverse pathways, these observations indicate that the most likely cause of the mating deficiency in met(-) cells is failure to methylate a component of the U. maydis pheromone signal transduction pathway.