Alternative oxidase: a respiratory electron transport chain pathway essential for maintaining photosynthetic performance during drought stress

2016 ◽  
Vol 157 (3) ◽  
pp. 322-337 ◽  
Author(s):  
Greg C. Vanlerberghe ◽  
Greg D. Martyn ◽  
Keshav Dahal
Keyword(s):  
Drought Stress ◽  
Electron Transport ◽  
Electron Transport Chain ◽  
Alternative Oxidase ◽  
Photosynthetic Performance ◽  
Transport Chain ◽  
Respiratory Electron Transport

scholarly journals Involvement of a G Protein Regulatory Circuit in Alternative Oxidase Production in Neurospora crassa

2019 ◽  
Vol 9 (10) ◽  
pp. 3453-3465 ◽  
Author(s):  
Natasa Bosnjak ◽  
Kristina M. Smith ◽  
Iman Asaria ◽  
Adrian Lahola-Chomiak ◽  
Nishka Kishore ◽  
...  
Keyword(s):  
Electron Transport ◽  
Neurospora Crassa ◽  
G Protein ◽  
Translational Control ◽  
Electron Transport Chain ◽  
Alternative Oxidase ◽  
G Protein Signaling ◽  
Mrna Levels ◽  
Protein Signaling ◽  
Transport Chain

The Neurospora crassa nuclear aod-1 gene encodes an alternative oxidase that functions in mitochondria. The enzyme provides a branch from the standard electron transport chain by transferring electrons directly from ubiquinol to oxygen. In standard laboratory strains, aod-1 is transcribed at very low levels under normal growth conditions. However, if the standard electron transport chain is disrupted, aod-1 mRNA expression is induced and the AOD1 protein is produced. We previously identified a strain of N. crassa, that produces high levels of aod-1 transcript under non-inducing conditions. Here we have crossed this strain to a standard lab strain and determined the genomic sequences of the parents and several progeny. Analysis of the sequence data and the levels of aod-1 mRNA in uninduced cultures revealed that a frameshift mutation in the flbA gene results in the high uninduced expression of aod-1. The flbA gene encodes a regulator of G protein signaling that decreases the activity of the Gα subunit of heterotrimeric G proteins. Our data suggest that strains with a functional flbA gene prevent uninduced expression of aod-1 by inactivating a G protein signaling pathway, and that this pathway is activated in cells grown under conditions that induce aod-1. Induced cells with a deletion of the gene encoding the Gα protein still have a partial increase in aod-1 mRNA levels, suggesting a second pathway for inducing transcription of the gene in N. crassa. We also present evidence that a translational control mechanism prevents production of AOD1 protein in uninduced cultures.

scholarly journals Improved photosynthetic capacity and photosystem I oxidation via heterologous metabolism engineering in cyanobacteria

2021 ◽  
Vol 118 (11) ◽  
pp. e2021523118
Author(s):  
María Santos-Merino ◽  
Alejandro Torrado ◽  
Geoffry A. Davis ◽  
Annika Röttig ◽  
Thomas S. Bibby ◽  
...  
Keyword(s):  
Cytochrome P450 ◽  
Electron Transport ◽  
Photosystem I ◽  
Metabolic Pathways ◽  
Electron Transport Chain ◽  
Photosynthetic Apparatus ◽  
Photosynthetic Performance ◽  
Cytochrome P450 Activity ◽  
Transport Chain ◽  
Source Sink

Cyanobacteria must prevent imbalances between absorbed light energy (source) and the metabolic capacity (sink) to utilize it to protect their photosynthetic apparatus against damage. A number of photoprotective mechanisms assist in dissipating excess absorbed energy, including respiratory terminal oxidases and flavodiiron proteins, but inherently reduce photosynthetic efficiency. Recently, it has been hypothesized that some engineered metabolic pathways may improve photosynthetic performance by correcting source/sink imbalances. In the context of this subject, we explored the interconnectivity between endogenous electron valves, and the activation of one or more heterologous metabolic sinks. We coexpressed two heterologous metabolic pathways that have been previously shown to positively impact photosynthetic activity in cyanobacteria, a sucrose production pathway (consuming ATP and reductant) and a reductant-only consuming cytochrome P450. Sucrose export was associated with improved quantum yield of phtotosystem II (PSII) and enhanced electron transport chain flux, especially at lower illumination levels, while cytochrome P450 activity led to photosynthetic enhancements primarily observed under high light. Moreover, coexpression of these two heterologous sinks showed additive impacts on photosynthesis, indicating that neither sink alone was capable of utilizing the full “overcapacity” of the electron transport chain. We find that heterologous sinks may partially compensate for the loss of photosystem I (PSI) oxidizing mechanisms even under rapid illumination changes, although this compensation is incomplete. Our results provide support for the theory that heterologous metabolism can act as a photosynthetic sink and exhibit some overlapping functionality with photoprotective mechanisms, while potentially conserving energy within useful metabolic products that might otherwise be “lost.”

scholarly journals Roles of Alanine Dehydrogenase and Induction of Its Gene inMycobacterium smegmatisunder Respiration-Inhibitory Conditions

2018 ◽  
Vol 200 (14) ◽  
Author(s):  
Ji-A Jeong ◽  
Sae Woong Park ◽  
Dahae Yoon ◽  
Suhkmann Kim ◽  
Ho-Young Kang ◽  
...  
Keyword(s):  
Electron Transport ◽  
Mycobacterium Smegmatis ◽  
Electron Transport Chain ◽  
Specific Inhibitor ◽  
Expression Level ◽  
Growth Defect ◽  
Content Type ◽  
Alanine Dehydrogenase ◽  
Transport Chain ◽  
Respiratory Electron Transport

ABSTRACTHere we demonstrated that the inhibition of electron flux through the respiratory electron transport chain (ETC) by either the disruption of the gene for the major terminal oxidase (aa3cytochromecoxidase) or treatment with KCN resulted in the induction ofaldencoding alanine dehydrogenase inMycobacterium smegmatis. A decrease in functionality of the ETC shifts the redox state of the NADH/NAD+pool toward a more reduced state, which in turn leads to an increase in cellular levels of alanine by Ald catalyzing the conversion of pyruvate to alanine with the concomitant oxidation of NADH to NAD+. The induction ofaldexpression under respiration-inhibitory conditions inM. smegmatisis mediated by the alanine-responsive AldR transcriptional regulator. The growth defect ofM. smegmatisby respiration inhibition was exacerbated by inactivation of thealdgene, suggesting that Ald is beneficial toM. smegmatisin its adaptation and survival under respiration-inhibitory conditions by maintaining NADH/NAD+homeostasis. The low susceptibility ofM. smegmatistobcc1complex inhibitors appears to be, at least in part, attributable to the high expression level of thebdquinol oxidase inM. smegmatiswhen thebcc1-aa3branch of the ETC is inactivated.IMPORTANCEWe demonstrated that the functionality of the respiratory electron transport chain is inversely related to the expression level of thealdgene encoding alanine dehydrogenase inMycobacterium smegmatis. Furthermore, the importance of Ald in NADH/NAD+homeostasis during the adaptation ofM. smegmatisto severe respiration-inhibitory conditions was demonstrated in this study. On the basis of these results, we propose that combinatory regimens including both an Ald-specific inhibitor and respiration-inhibitory antitubercular drugs such as Q203 and bedaquiline are likely to enable a more efficient therapy for tuberculosis.

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