This Key Event Relationship is licensed under the Creative Commons BY-SA license. This license allows reusers to distribute, remix, adapt, and build upon the material in any medium or format, so long as attribution is given to the creator. The license allows for commercial use. If you remix, adapt, or build upon the material, you must license the modified material under identical terms.

Relationship: 3557

Title

A descriptive phrase which clearly defines the two KEs being considered and the sequential relationship between them (i.e., which is upstream, and which is downstream). More help

Decrease, Photosynthesis leads to Decrease in mitochondrial oxidative phosphorylation

Upstream event

The causing Key Event (KE) in a Key Event Relationship (KER). More help

Decrease, Photosynthesis

Downstream event

The responding Key Event (KE) in a Key Event Relationship (KER). More help

Decrease in mitochondrial oxidative phosphorylation

Key Event Relationship Overview

The utility of AOPs for regulatory application is defined, to a large extent, by the confidence and precision with which they facilitate extrapolation of data measured at low levels of biological organisation to predicted outcomes at higher levels of organisation and the extent to which they can link biological effect measurements to their specific causes.Within the AOP framework, the predictive relationships that facilitate extrapolation are represented by the KERs. Consequently, the overall WoE for an AOP is a reflection in part, of the level of confidence in the underlying series of KERs it encompasses. Therefore, describing the KERs in an AOP involves assembling and organising the types of information and evidence that defines the scientific basis for inferring the probable change in, or state of, a downstream KE from the known or measured state of an upstream KE. More help

AOPs Referencing Relationship

AOP Name	Adjacency	Weight of Evidence	Quantitative Understanding	Point of Contact	Author Status	OECD Status
Binding to plastoquinone B site leading to decreased population growth rate via photosystem II inhibition	adjacent	Moderate	Moderate	Li Xie (send email)	Under development: Not open for comment. Do not cite

Taxonomic Applicability

Latin or common names of a species or broader taxonomic grouping (e.g., class, order, family) that help to define the biological applicability domain of the KER.In general, this will be dictated by the more restrictive of the two KEs being linked together by the KER. More help

Term	Scientific Term	Evidence	Link
Lemna minor	Lemna minor	High	NCBI
Arabidopsis thaliana	Arabidopsis thaliana	High	NCBI
Chlamydomonas reinhardtii	Chlamydomonas reinhardtii	High	NCBI

Sex Applicability

An indication of the the relevant sex for this KER. More help

Sex	Evidence
Unspecific	High

Life Stage Applicability

An indication of the the relevant life stage(s) for this KER. More help

Term	Evidence
All life stages	High

Key Event Relationship Description

Provides a concise overview of the information given below as well as addressing details that aren’t inherent in the description of the KEs themselves. More help

The KER between decreased photosynthesis and decreased mitochondrial oxidative phosphorylation (OXPHOS) reflects the tight metabolic coupling between chloroplast carbon fixation and mitochondrial respiration in photosynthetic eukaryotes. Reduced photosynthetic electron transport lowers ATP and NADPH production and limits CO₂ assimilation, thereby decreasing carbohydrate availability for mitochondrial respiration (Maxwell & Johnson, 2000). As a consequence, reduced supply of pyruvate and tricarboxylic acid (TCA) cycle intermediates constrains electron input into the mitochondrial electron transport chain, diminishing OXPHOS activity and ATP synthesis (Milligan et al., 2015). Furthermore, disruption of photosynthetic redox balance can alter respiratory flux and mitochondrial energy metabolism, reinforcing cross-organelle energetic dependence.

Evidence Collection Strategy

Include a description of the approach for identification and assembly of the evidence base for the KER. For evidence identification, include, for example, a description of the sources and dates of information consulted including expert knowledge, databases searched and associated search terms/strings. Include also a description of study screening criteria and methodology, study quality assessment considerations, the data extraction strategy and links to any repositories/databases of relevant references.Tabular summaries and links to relevant supporting documentation are encouraged, wherever possible. More help

Evidence was collected through targeted literature searches linking photosynthetic inhibition to respiratory and mitochondrial endpoints, including oxygen consumption, ATP synthesis rates, and OXPHOS enzyme activity. Screening incorporated studies measuring both chlorophyll fluorescence (Fv/Fm) and mitochondrial respiration parameters to ensure mechanistic continuity between reduced carbon fixation and diminished oxidative phosphorylation.

Evidence Supporting this KER

Addresses the scientific evidence supporting KERs in an AOP setting the stage for overall assessment of the AOP. More help

Experimental evidence demonstrates that inhibition of photosynthesis reduces mitochondrial respiration due to diminished carbon substrate supply. Studies measuring chlorophyll fluorescence (Fv/Fm) and carbon fixation show that reduced photosynthetic performance directly limits carbohydrate production (Maxwell & Johnson, 2000). In phytoplankton and plants, decreased ¹⁴C assimilation is associated with reduced respiratory oxygen consumption, reflecting constrained substrate flow into the tricarboxylic acid cycle (Milligan et al., 2015). Additionally, stress-induced impairment of photosynthetic electron transport alters cellular redox balance, influencing mitochondrial metabolic flux. Together, these findings support a mechanistic link between decreased photosynthetic carbon assimilation and reduced mitochondrial oxidative phosphorylation activity.

Biological Plausibility

Addresses the biological rationale for a connection between KEupstream and KEdownstream. This field can also incorporate additional mechanistic details that help inform the relationship between KEs, this is useful when it is not practical/pragmatic to represent these details as separate KEs due to the difficulty or relative infrequency with which it is likely to be measured. More help

Substantial evidence demonstrates tight functional integration between chloroplast photosynthesis and mitochondrial oxidative phosphorylation in photosynthetic eukaryotes. Photosynthetically derived carbohydrates provide the primary substrates for glycolysis and the tricarboxylic acid (TCA) cycle, which generate NADH and FADH₂ for the mitochondrial electron transport chain (Raghavendra & Padmasree, 2003). When photosynthetic carbon assimilation declines, respiratory substrate availability is reduced, resulting in decreased mitochondrial electron transport and ATP synthesis (Noguchi & Yoshida, 2008). In addition, chloroplast–mitochondria redox shuttles coordinate cellular NAD(P)H balance; disruption of photosynthetic electron flow alters mitochondrial respiratory flux and energy homeostasis (Noctor et al., 2007). Together, these studies support a mechanistic linkage whereby decreased photosynthesis constrains mitochondrial oxidative phosphorylation through substrate limitation and redox coupling.

Empirical Evidence

Provides specific (citable) evidence that supports the idea of a change in the upstream KE (KEupstream) leading to, or being associated with, a subsequent change in the downstream KE (KEdownstream), assuming the perturbation of KEupstream is sufficient. More help

The empirical support of this KER is considered moderate.

Rationale: A substantial body of experimental evidence demonstrates incidence and temporal concordance between reduced photosynthetic carbon assimilation and decreased mitochondrial respiration in photosynthetic organisms. However, fewer studies directly quantify oxidative phosphorylation parameters (e.g., ATP synthesis rate, respiratory control ratio) alongside photosynthetic inhibition, limiting quantitative resolution.

Evidence

Dose concordance: In plant mesophyll cells, inhibition of photosynthesis using PSII inhibitors (e.g., DCMU) reduces carbohydrate production and is accompanied by decreases in mitochondrial respiratory flux and coupled oxidative metabolism (Padmasree et al., 2001; Noguchi & Yoshida, 2008).

Incidence concordance: Experimental reductions in carbon fixation consistently correspond with reduced mitochondrial oxygen consumption due to limited substrate flow into glycolysis and the TCA cycle (Raghavendra, 1994; Raghavendra & Padmasree, 2003).

Temporal concordance: Respiratory adjustments occur rapidly following changes in photosynthetic performance, particularly under illuminated conditions where chloroplast–mitochondrial coupling is strongest (Noguchi & Yoshida, 2008).

Mechanistic concordance: Chloroplast–mitochondria metabolite exchange and redox shuttling provide a mechanistic basis whereby reduced photosynthetic ATP/NADPH production constrains mitochondrial electron transport and oxidative phosphorylation (Noctor et al., 2007; Igamberdiev, 2023).

Uncertainties and Inconsistencies

Addresses inconsistencies or uncertainties in the relationship including the identification of experimental details that may explain apparent deviations from the expected patterns of concordance. More help

Uncertainty arises because mitochondrial respiration can be partially maintained through alternative substrates (e.g., stored carbohydrates or photorespiration), buffering short-term declines in photosynthesis. Additionally, some studies report compensatory increases in respiratory activity under stress. Direct measurements of OXPHOS parameters are limited, reducing quantitative precision of this linkage.

Known modulating factors

This table captures specific information on the MF, its properties, how it affects the KER and respective references.1.) What is the modulating factor? Name the factor for which solid evidence exists that it influences this KER. Examples: age, sex, genotype, diet 2.) Details of this modulating factor. Specify which features of this MF are relevant for this KER. Examples: a specific age range or a specific biological age (defined by...); a specific gene mutation or variant, a specific nutrient (deficit or surplus); a sex-specific homone; a certain threshold value (e.g. serum levels of a chemical above...) 3.) Description of how this modulating factor affects this KER. Describe the provable modification of the KER (also quantitatively, if known). Examples: increase or decrease of the magnitude of effect (by a factor of...); change of the time-course of the effect (onset delay by...); alteration of the probability of the effect; increase or decrease of the sensitivity of the downstream effect (by a factor of...) 4.) Provision of supporting scientific evidence for an effect of this MF on this KER. Give a list of references. More help

Modulating Factor (MF)	MF Specification	Effect(s) on the KER	Reference(s)
Light intensity	Low vs. high irradiance; photoinhibitory vs. optimal light	High light amplifies chloroplast–mitochondria redox coupling and increases respiratory demand; low light reduces substrate flux, weakening the linkage	Noguchi & Yoshida, 2008
Carbon availability	CO₂ concentration; carbohydrate reserves	Low CO₂ or depleted carbohydrate pools strengthen substrate limitation, enhancing the impact of reduced photosynthesis on OXPHOS	Raghavendra & Padmasree, 2003
Developmental stage	Young vs. mature leaves/cells	Younger tissues with higher metabolic turnover show stronger coupling between carbon fixation and respiration	Padmasree et al., 2001
Alternative oxidase (AOX) activity	Induction of AOX pathway under stress	AOX can partially uncouple electron transport from ATP production, modifying the magnitude of OXPHOS reduction	Noctor et al., 2007
Temperature	Suboptimal vs. optimal temperature	Temperature affects both photosynthesis and mitochondrial enzyme kinetics, altering respiratory compensation capacity	Noguchi & Yoshida, 2008
Nutrient status	Nitrogen or phosphate limitation	Nutrient stress modifies carbon allocation and respiratory metabolism, influencing the strength of organelle coupling	Raghavendra, 1994
Stress-induced ROS	Elevated ROS levels	Oxidative stress can impair both chloroplast and mitochondrial function, potentially amplifying the KER	Igamberdiev, 2023

Quantitative Understanding of the Linkage

Captures information that helps to define how much change in the upstream KE, and/or for how long, is needed to elicit a detectable and defined change in the downstream KE. More help

The quantitative understanding of this KER is moderate

Rationale: few experimental studies demonstrate that reductions in photosynthetic carbon assimilation (via chemical inhibition or metabolic perturbation) coincide with decreases in mitochondrial respiratory activity in iprimary producers. While dose–response characterization of mitochondrial OXPHOS secondary to photosynthesis inhibition is not common, proportional decreases in respiration align with graded photosynthetic impairment.

Dose-reponse concordance: In Lemna minor exposed to gamma radiation for 7 days, CO₂ uptake declined dose-dependently (EDR10 = 2.8 mGy/h; EDR50 = 53.2 mGy/h), while mitochondrial membrane potential (MMP, proxy for OXPHOS) decreased at higher thresholds (EDR10 = 21.8 mGy/h; EDR50 = 144.7 mGy/h). The lower sensitivity threshold for photosynthesis relative to MMP supports upstream–downstream quantitative concordance between decreased carbon assimilation and mitochondrial dysfunction (Xie et al., 2019).

Temporal concordance: Both photosynthesis endpoints and mitochondrial membrane potential (MMP) were measured after the same 7-day exposure period. Declines in CO₂ uptake and PSII efficiency co-occurred with significant reductions in MMP at ≥24 mGy/h, demonstrating coordinated impairment of chloroplast and mitochondrial function within the same biological timeframe (Xie et al., 2019).

Response-response Relationship

Provides sources of data that define the response-response relationships between the KEs. More help

The biological plausibility of this KER is high due to the fundamental metabolic coupling between chloroplasts and mitochondria in photosynthetic eukaryotes. Photosynthesis generates carbohydrates that serve as substrates for glycolysis and the tricarboxylic acid (TCA) cycle, providing reducing equivalents (NADH, FADH₂) to the mitochondrial electron transport chain (Milligan et al., 2015). Reductions in PSII efficiency and carbon fixation therefore constrain respiratory substrate availability (Maxwell & Johnson, 2000). Furthermore, chloroplast and mitochondrial redox states are interconnected through metabolite exchange and shared energy demands, linking photosynthetic performance with respiratory flux. Disruption of photosynthetic electron transport alters cellular redox balance and impacts downstream mitochondrial ATP production (Broser et al., 2011; Delieu & Walker, 1981).

Time-scale

Information regarding the approximate time-scale of the changes in KEdownstream relative to changes in KEupstream (i.e., do effects on KEdownstream lag those on KEupstream by seconds, minutes, hours, or days?). More help

The time-scale of this KER is rapid under illuminated conditions. Experimental inhibition of photosynthesis leads to measurable decreases in mitochondrial respiratory flux within minutes to hours, reflecting immediate limitation of carbon substrates and redox imbalance (Noguchi & Yoshida, 2008; Padmasree et al., 2001). Sustained inhibition can prolong respiratory suppression.

Known Feedforward/Feedback loops influencing this KER

Define whether there are known positive or negative feedback mechanisms involved and what is understood about their time-course and homeostatic limits. More help

Reduced photosynthesis limits carbohydrate supply to mitochondria, decreasing OXPHOS and ATP production. Lower ATP availability can further constrain chloroplast metabolism, reinforcing energetic limitation (Raghavendra & Padmasree, 2003). Additionally, redox imbalance promotes reactive oxygen species formation, which can impair both chloroplast and mitochondrial function, amplifying metabolic suppression (Noctor et al., 2007).

Domain of Applicability

A free-text section of the KER description that the developers can use to explain their rationale for the taxonomic, life stage, or sex applicability structured terms. More help

Taxonomic applicability: This KER applies broadly to oxygenic photosynthetic eukaryotes in which chloroplast carbon fixation supplies substrates for mitochondrial respiration. It is strongly supported in higher plants, green algae, and photosynthetic protists, where chloroplast–mitochondria metabolic coupling is well documented (Raghavendra & Padmasree, 2003; Noguchi & Yoshida, 2008). Applicability to cyanobacteria is limited because respiration and photosynthesis occur within the same cellular membrane system rather than in distinct organelles.

Sex applicability: Not sex-specific. The metabolic linkage between photosynthesis and mitochondrial oxidative phosphorylation is fundamental to cellular bioenergetics and operates similarly in male and female individuals of dioecious plants. In unicellular algae and clonal macrophytes, sex differentiation is generally not relevant.

Life-stage applicability: Applicable across all photosynthetically active life stages, including vegetative cells, seedlings, mature leaves, and reproductive tissues that perform photosynthesis. The magnitude of coupling may vary with developmental stage due to differences in metabolic demand, carbohydrate storage capacity, and respiratory flexibility (Padmasree et al., 2001).

Chemical domain: Relevant to chemicals that reduce photosynthetic carbon assimilation, including PSII inhibitors (e.g., triazines, phenylureas), PSI inhibitors, electron transport disruptors, pigment synthesis inhibitors, and carbon fixation inhibitors. Chemicals acting exclusively on mitochondria without affecting photosynthesis fall outside this KER. Indirect stressors (e.g., light deprivation, CO₂ limitation) are also within scope if they reduce carbon fixation and secondarily constrain mitochondrial oxidative phosphorylation.

References

List of the literature that was cited for this KER description. More help

Broser, M., Glöckner, C., Gabdulkhakov, A., Guskov, A., Buchta, J., Kern, J., Müh, F., Dau, H., Saenger, W., & Zouni, A. (2011). Structural basis of cyanobacterial photosystem II inhibition by the herbicide terbutryn. Journal of Biological Chemistry, 286(18), 15964–15972.

Delieu, T., & Walker, D.A. (1981). Polarographic measurement of photosynthetic oxygen evolution by leaf discs. New Phytologist, 89(2), 165–178.

Igamberdiev, A.U. (2023). Mitochondria in photosynthetic cells: Coordinating redox and energy metabolism. Plant Physiology, 191(4), 2104–2120.

Maxwell, K., & Johnson, G.N. (2000). Chlorophyll fluorescence—a practical guide. Journal of Experimental Botany, 51(345), 659–668.

Milligan, A.J., Halsey, K.H., & Behrenfeld, M.J. (2015). Advancing interpretations of ¹⁴C-uptake measurements in the context of phytoplankton physiology and ecology. Journal of Plankton Research, 37(4), 692–698.

Noctor, G., De Paepe, R., & Foyer, C.H. (2007). Mitochondrial redox biology and homeostasis in plants. Trends in Plant Science, 12(3), 125–134.

Noguchi, K., & Yoshida, K. (2008). Interaction between photosynthesis and respiration in illuminated leaves. Mitochondrion, 8(1), 87–99.

Padmasree, K., Padmavathi, L., & Raghavendra, A.S. (2001). Essentiality of mitochondrial oxidative metabolism for photosynthetic performance in plant cells. Plant Physiology, 125(2), 617–626.

Raghavendra, A.S. (1994). Interdependence of photosynthesis and respiration in plant cells. Photosynthesis Research, 38, 3–14.

Raghavendra, A.S., & Padmasree, K. (2003). Beneficial interactions of mitochondrial metabolism with photosynthetic carbon assimilation. Trends in Plant Science, 8(11), 546–553.

Xie, L., Solhaug, K.A., Song, Y., Brede, D.A., Lind, O.C., Salbu, B., & Tollefsen, K.E. (2019). Modes of action and adverse effects of gamma radiation in an aquatic macrophyte Lemna minor. Science of the Total Environment, 680, 23–34.