Effect of cyclic AMP on catabolite-repressed zoosporangial formation in Phytophthora capsici

1977 ◽  
Vol 55 (7) ◽  
pp. 840-843 ◽  
Author(s):  
M. Yoshikawa ◽  
H. Masago

Zoosporangial formation in Phytophthora capsici was sensitively inhibited by glucose and other catabolites including sugars, citric acid cycle acids, and amino acids, but was only slightly inhibited by 3-O-methylglucose and 2-deoxyglucose and by other seemingly weak catabolites. The inhibitions were specifically prevented by cyclic AMP among the various related nucleotides evaluated. The reversing effect by cyclic AMP was observed only on zoosporangial formation that was partially repressed by catabolites, but the completely repressed zoosporangial formation could not be reversed by cyclic AMP. Furthermore, cyclic AMP failed in reversing zoosporangial formation that was inhibited by antibiotics such as antimycin A and cycloheximide. The results suggested that the initiation of zoosporangial formation in the fungus is under the control of catabolite repression that is mediated by cyclic AMP.

1957 ◽  
Vol 35 (6) ◽  
pp. 365-371 ◽  
Author(s):  
E. Bilinski ◽  
W. B. McConnell

Glutamic acid, aspartic acid, and threonine isolated from the gluten of wheat plants to which acetate-1-C14 or -2-C14 was administered during growth have been degraded to determine the complete intramolecular distribution of C14. Sixty-three per cent of the activity in glutamic acid arising from acetate-1-C14 was in carbon-5 and 20% in carbon-1; glutamic acid from acetate-2-C14 contained 43% of the activity in carbon-4 and about 18% in each of carbons 2 and 3. Acetate-1-C14 resulted in labelling largely in the terminal carbons of aspartic acid, and acetate-2-C14 preferentially labelled the internal carbons. The results show that the Krebs' citric acid cycle provides a major pathway for the biosynthesis of the dicarboxylic amino acids of wheat gluten.Striking parallelism in the intramolecular distribution of carbon-14 in aspartic acid and threonine demonstrates that these amino acids are closely linked biosynthetically and is in accord with the idea that aspartic acid provides the carbon skeleton for threonine.


1966 ◽  
Vol 12 (1) ◽  
pp. 1-4 ◽  
Author(s):  
Edwin C. Gangloff

All of the intermediates of the citric acid cycle are shown to be present in the mycelium of 6-day cultures of P. blakesleeanus grown on glucose and on ammonium sulfate, and fed non-radioactive acetate on the fourth and fifth days and acetate-1-C14 on the fifth day of incubation.The concentration of organic acids and certain amino acids, and their specific activity is reported. The high activity of the latter is thought to indicate the presence of a highly labeled pool of nitrogen compounds persisting from the early anabolic reactions after acetate-1-C14 administration.


1983 ◽  
Vol 3 (4) ◽  
pp. 498-506 ◽  
Author(s):  
Jean Holowach Thurston ◽  
Richard E. Hauhart ◽  
James A. Schiro

The recovery of weanling mice from insulin-induced hypoglycemic stupor–coma after injection of sodium -l(+)-lactate (18 mmol/kg) was as rapid (10 min) as in litter-mates treated with glucose (9 mmol/kg). Stimulated by this dramatic action, we studied the effects of lactate injection on brain carbohydrate and energy metabolism in normal and hypoglycemic mice; blood and liver tissue were also studied. Ten minutes after lactate injection in normal mice, plasma lactate levels increased by 15 mmol/L; plasma glucose levels were unchanged, but the β-hydroxybutyrate concentration fell 59%. In the brains of these animals, glucose levels increased 2.3-fold, and there were significant increases in brain glycogen (10%), glucose-6-phosphate (27%), lactate (68%), pyruvate (37%), citrate (12%), and malate (19%); the increase in α-ketoglutarate (32%) was not significant. Lactate injection reduced the cerebral glucose-use rate 40%. These changes were not due to lactate-induced increases in blood [HCO−3] and pH (examined by injection of 15 mmol/kg sodium bicarbonate). Although lactate injection of hypoglycemic mice doubled levels of glucose in plasma and brain (not significant) and most of the cerebral glycolytic intermediates, values were far below normal (still in the range seen in hypoglycemic animals). By contrast, citrate and α-ketoglutarate levels returned to normal; the large increase in malate was not significant. Reduced glutamate levels increased to normal, and elevated aspartate levels fell below normal. Thus, recovery from hypoglycemic stupor does not necessarily depend on normal levels of plasma and/or brain glucose (or glycolytic intermediates). Near normal levels of the Krebs citric acid cycle intermediates suggest that changes in these metabolites, amino acids, or derived substrates relate to the dramatic recovery of hypoglycemic mice after lactate injection.


2011 ◽  
Vol 24 (No. 1) ◽  
pp. 1-10
Author(s):  
J. Velíšek ◽  
K. Cejpek

This review article gives a survey of principal pathways that lead to the biosynthesis of the proteinogenic amino acids of the glutamic acid group (glutamic acid, glutamine, proline, arginine) and aspartic acid group (aspartic acid, asparagine, threonine, methionine, lysine, isoleucine) starting with oxaloacetic acid from the citric acid cycle. There is an extensive use of reaction schemes, sequences, and mechanisms with the enzymes involved and detailed explanations using sound chemical principles and mechanisms.


PEDIATRICS ◽  
1959 ◽  
Vol 23 (1) ◽  
pp. 245-251
Author(s):  
Meredith N. Runner

Fasting for 24 hours during the ninth day of pregnancy resulted in 22% of the fetuses having either cranioschisis or deformed ribs or both at 18 days post coitum. The fasting treatment affected neither the frequency of pregnancies following matings nor the incidence of prenatal mortality. Fetuses were protected from the fasting effect by relatively small quantities of a variety of nutrients, i.e., glucose, ketone-body or amino acids administered by stomach tube during the fasting period. The array of protective compounds suggested that they acted by supplying substrate for the citric acid cycle. Four teratogenic treatments (insulin, iodoacetate, x-methylfolic acid and fasting) produced similar abnormalities of development. A metabolic scheme is presented to suggest that each of these agents may interfere with reactions in the citric acid cycle. Administration of nutrients during the fasting period and use of teratogenic agents have provided circumstantial evidence that carbohydrate metabolism may be selectively critical for morphogenesis of embryonic neural tube and for differentiation of precartilaginous mesenchyme.


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