Modeling the Interplay between Photosynthesis, CO2 Fixation, and the Quinone Pool in a Purple Non-Sulfur Bacterium
read more
Citations
OptFill: A Tool for Infeasible Cycle-Free Gapfilling of Stoichiometric Metabolic Models.
An integrated computational and experimental studyto investigate Staphylococcus aureus metabolism
Synergistic Experimental and Computational Approach Identifies Novel Strategies for PHB Overproduction
References
Phototrophic extracellular electron uptake is linked to carbon dioxide fixation in the bacterium Rhodopseudomonas palustris.
Metabolic engineering of the pentose phosphate pathway for enhanced limonene production in the cyanobacterium Synechocysti s sp. PCC 6803
Reconstruction and Comparison of the Metabolic Potential of Cyanobacteria Cyanothece sp. ATCC 51142 and Synechocystis sp. PCC 6803
Predicting Gene Essentiality Using Genome-Scale in Silico Models
Metabolic network modeling of redox balancing and biohydrogen production in purple nonsulfur bacteria
Related Papers (5)
Optimization of ATP Synthase c-Rings for Oxygenic Photosynthesis.
Anaerobic respiration in the Rhodospirillaceae: characterisation of pathways and evaluation of roles in redox balancing during photosynthesis
Frequently Asked Questions (17)
Q2. What have the authors stated for future works in "Modeling the interplay between photosynthesis, co2 fixation, and the quinone pool in a purple non- sulfur bacterium" ?
Future experimental work will be conducted to measure the electron transport rate, intracellular ATP concentration, and RuBisCO gene expression across different quinone redox states to strengthen the proposed hypothesis and further refine the model.
Q3. What is the effect of the redox state on the CBB system?
Predictions also indicated that the extent of CO2 fixation is dependent on the amount of ATP present, with the quinone redox state acting as a feed-forward signal to the CBB system.
Q4. What was the effect of the quinols on growth?
During initial phototrophic growth simulations, growth on any of the four carbon sources (acetate, fumarate, succinate, and butyrate) was observed to be hindered due to the accumulation of excess quinols formed in the TCA cycle.
Q5. What is the role of the ribulose carboxylase/oxygenase?
CO2-fixation using the enzyme ribulose-1,5-biphosphate carboxylase/oxygenase (RuBisCO), nitrogen-fixation through the enzyme nitrogenase12, and supplementation with an electron acceptor (e.g., trimethylamine-N-oxide (TMAO))15 all prevent the inhibitory accumulation of excess reducing agents.
Q6. What is the effect of the light uptake rate on the quinol sink?
Although the model predicted that the rate of CO2 fixation increased linearly with light uptake rate, kinetic and thermodynamic constrains on the highly inefficient CO2-fixing RuBisCO enzyme50 hinders this process at high light uptake.
Q7. Who provided funding to support this work?
Funding to support this work was provided by University of Nebraska-Lincoln Faculty Startup Grant and Nebraska Center for Energy Sciences Research (NCESR) to Rajib Saha.
Q8. What is the redox state of the quinone oxidoreductas?
In this study, a genome-scale metabolic network (iRpa940) was used to propose a system-wide mechanistic model of the interactive system that includes photosynthesis, carbon dioxide fixation, and the quinone redox state.
Q9. What was used to fill the gaps in the network?
the ModelSEED database33 was used to fill the gaps in the network, and a biomass producing model was generated in KBase32.
Q10. How many reactions were annotated during the gap-filling procedure?
Out of the 478 reactions added during gap-filling, 368 were annotated using information from organism-specific databases (see Methods).
Q11. What is the role of the Calvin-Benson-Bassham cycle?
Several studies conducted on R. palustris showed that in addition to the Calvin-Benson-Bassham (CBB) cycle’s role of carbon assimilation during autotrophic growth, the pathway plays a major role in maintaining redox balance under heterotrophic conditions10,12–14.
Q12. What is the redox state of the quinone pool?
Based on this analysis, it is hypothesized that the quinone redox state acts as a feed-forward controller of the CBB pathway, signaling the amount of ATP available.
Q13. What is the function of the quinone redox state?
the quinone redox state is predicted to act as a feed-forward controller to the energetically expensive CBB pathway, indicating how much ATP is available at a given condition.
Q14. What is the effect of the quinol sink on cellular growth?
After the model indicated the presence of an unidentified quinol sink, in silico simulations were combined with published in vivo flux measurements13,14 to study the effect (and the extent) of the quinone redox state on cellular growth, electron transport rate, and CO2 fixation.
Q15. What was the rate of quinone reduction in the TCA cycle?
The quinol sink reaction was treated as a parameter in the model and pFBA simulations were conducted at varying quinol oxidation (sink) rates to determine how light uptake (i.e. Electron Transport Rate or ETR), growth, and CO2 fixation are affected by changes in the quinone redox state (Fig. 2).
Q16. What was the rate of quinol oxidization in the reaction center?
Flux analysis of the electron transport chain (ETC) revealed that the rate of quinol oxidization through the cytochrome bc1 complex was equivalent to the rate of quinone reduction in the Reaction center (RC).
Q17. What is the role of redox state in the ATP cycle?
These results suggest that redox state acts as a feed-forward controller of the highly energy-demanding CBB cycle by regulating the rate of light-generated ATP.