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At least 523 records · Page 29Linked to original sources
PubMed1987

Identification of the phosphate-translocator from maize mesophyll chloroplasts.

Intact maize mesophyll chloroplasts have been isolated in yields of up to 10 mg of chlorophyll per preparation. The chloroplasts were able to reduce 3-phosphoglycerate at a rate of 2.4 mumol of oxygen/min/mg of chlorophyll. This activity was inhibited by preincubating the intact chloroplasts with pyridoxal 5-phosphate. Chloroplast envelopes have been prepared and the protein profile has been obtained on SDS-polyacrylamide gels. The phosphate-translocator from the chloroplast envelope has been identified as a 30kDa polypeptide.

Carrier Proteins↗
PubMed1987

Photoreductive path of carbon fixation in green plant photosynthesis. Reaction pathway of six-carbon ribulose 1,5-bisphosphate carboxylation adduct intermediate.

In this paper we examine the six-carbon intermediate pathway of ribulose 1,5-bisphosphate (RuBP) carboxylation reaction in photosynthesis. Based on the observed reactions of purified RuBP carboxylase, mechanisms are described for carbon dioxide assimilation leading to the hydrolytic splitting of the six-carbon intermediate to two enzyme-bound glycerate-3-P (3-PGA) molecules. It is concluded that, under photosynthetic conditions, the reduction of enzyme-bound NADP+ by the chlorophyll is responsible for the rapid carboxylase turnover rate given by the lifetime, tau L = 0.4 s, which is nearly two orders of magnitude shorter than the corresponding value, tau D = 11 +/- 3 s, for the dark decay of enzyme-bound RuBP. The nocturnal inhibition and photoactivation of RuBP carboxylation are described in terms of the reversible light-dark cycles of the NADP+/NADPH redox couple and endogenous changes that accompany the 2-carboxy-D-arabinitol-1-phosphate binding to the enzyme active site.

Carbon↗
PubMed1988

Non-cyclic photoreductive carbon fixation in photosynthesis. Light and dark transients of the glycerate-3-P special pair.

It is demonstrated that carbon fixation in photosynthesis is regulated in two kinetically coupled pathways involving the specialized pair of non-equivalent, enzyme-bound glycerate-3-P (3-PGA) molecules obtained from ribulose 1,5-bisphosphate (RuBP) carboxylation in the light. A non-cyclic pathway is suggested (reaction 2) for the direct biosynthesis of sucrose from the 3-PGA obtained from C-3, C-4 and C-5 of the six-carbon carboxylation adduct. Concomitant to the appearance of sucrose as the principal product, the Mg2+-bound 3-PGA molecule formed from C-1, C-2 and C-2' of the C6 intermediate is released and subsequently reduced in regenerating the RuBP. It is proposed that the nocturnal inhibitor, 2-carboxyarabinitol-1-phosphate (1-PCA) is obtained from a condensation of 3-PGA and glyceraldehyde.

Carbon↗
PubMed1976

Effects of fructose-1,6-diphosphate administration on learning efficiency and time sense of the honey bee, Apis mellifica carnica.

In discrimination experiments honey bees had to decide between two glass dishes, one placed on a black cross, the other 40 cm away on a black square. In spontaneous selections the bees in 70% of all cases chose the black cross. The bees were then trained to search back and forth between the cross and the square until after 5 min sugar-water was given on the black square. Over a total of 5 learning trials, during which multiple decisions had been made by the searching insects, 96% of all choices were in favour of the black square. If 80 mM fructose-1,6-diphosphate (F-1,6-P2) in 1 M glucose had been ingested by the bees 30 min before the first spontaneous choice, learning was facilitated with 83% deciding in favour of the black square at the first trial compared with 46% of the controls (which had been fed on 1 M glucose only). In both groups of bees the same number of flight approches was made to the cross or square as made by the bees searching for 5 min before the reward was given. Thus no change in general activity or harvesting motivation appears to be induced by F-1,6-P2. When F-1,6-P2 had been given at the end of a successful learning series the bees favoured the black square for up to 3 days. In contrast to the controls no new incentive needed to be given during this period. Ingestion of other metabolites proved either ineffective, as in the case of fructose-6-phosphate or 5'-adenosine monophosphate, or, as observed after feeding citrate plus 3-phosphoglycerate, even reduced the performance. To test the effect of F-1,6P2 on the same time sense (circadian rhythm), bees were trained on three successive days to visit a feeding place at a specific time of day. The control bees which ingested only glucose on the evening of the 3rd day returned at their entrained 24-h interval on the 4th day. In contrast, the maximum frequency of appearance of bees fed on F-1,6-P2 was advanced by one hour, with minor appearance peaks at earlier hours of the day.

Animals↗
PubMed1976

Metabolic regulations of the rhythmic activity in pacemaker neurons. II. Metabolically induced conversions of beating to bursting pacemaker activity in isolated Aplysia neurons.

In pacemaker neurons of the sea hare Aplysia californica, isolated from their synaptic, ephaptic and humoral inputs, conversion of the regular beating to a bursting discharge pattern can be induced by certain cell metabolites. Administration of the phosphofructokinase (PFK) activator fructose-6-phosphate (F-6-P), or its nonmetabolizable analogue 1-deoxy-F-6-P, induced bursting discharges in R3, R5, R6 and R11 neurons, with spike doublets and triplets appearing transiently in the time pattern. With another PFK activitor, adenosine-5-monophosphate, only double spikes have been noted in R7, R8 and R14 neurons. Burst activity was induced also in the presence of the fructose-1,6-diphosphatase activators, citrate and 3-phosphoglycerate, in R9, R10 and R12 neurons. Cyclic 3',5'-AMP, which also activates the PFK (beside other effects on cellular metabolism), induced bursting discharges in all R3-R14 neurons. In contrast, the inhibitors of the PFK, citrate and ATP, decreased the spike activity of the bursting L3 and L6 neurons, even changing L3 neurons to the regular beating type. Among a variety of cell metabolites tested only pyruvate was able to induce a burst-like tendency in R9 neurons. The characteristic bursting patterns which appeared in the presence of the described metabolic effectors could not be duplicated by low Ca2+ and/or high K+ media nor by artificial shifts in membrane potential triggered by depolarizing and hyperpolarizing currents.

Adenosine Monophosphate↗
PubMed1976

Metabolic regulations of the rhythmic activity in pacemaker neurons. III. Neutralization of the pentylenetetrazol effect in regularly beating Aplysia neurons by metabolic modifiers.

In regular beating pacemaker neurons isolated from the sea hare Aplysia californica, 30-50 mM pentylenetetrazol (PTZ) induces spike doublets and triplets, multi-spike bursts, and paroxysmal depolarizing shifts. The development of the characteristic PTZ-induced changes in impluse pattern is preceded by a transient increase in discharge frequency and a reduction in after-hyperpolarization. According to earlier findings, the rhythmic spike activity of pacemaker neurons is governed by a phosphofructokinase-fructose-1,6-diphosphatase-mediated substrate cycle, the activation of which leads to the appearance of spike bursts. Inhibitory modifiers of this neuronal substrate cycle, such as citrate, ATP, and 3-phosphoglycerate, are able to neutralize the changes in the impluse characteristics occurring as the result of PTZ action. Since the reinitiated single-spike trains reverted again to the PTZ pattern following the further addition of activating modifiers, such as fructose-1,6-diphosphate or fructose-6-phosphate, it appears likely that PTZ exerts an influence on the metabolic reactions driving the rhythmic spike activity. In contrast to the reversible effects of the metabolic modifiers the conventional anti-convulsants, phenobarbital and pentobarbital, merely block all spike activity.

Adenosine Triphosphate↗