During carbon starvation, autophagy is associated with protein degradation and impact energy status by regulating alternative respiration via the ETF/ETFQO thro

Stomata control the exchange of CO₂ and water vapor in land plants. Thus, whereas a constant supply of CO₂ is required to maintain adequate rates of photosynthesis, the accompanying water losses must be tightly regulated to prevent dehydration and undesired metabolic changes. Accordingly, the uptake or release of ions and metabolites from guard cells is necessary to achieve normal stomatal function. The AtQUAC1, an R-type anion channel responsible for the release of malate from guard cells, is essential for efficient stomatal closure. Here, we demonstrate that mutant plants lacking AtQUAC1 accumulated higher levels of malate and fumarate. These mutant plants not only display slower stomatal closure in response to increased CO₂ concentration and dark but are also characterized by improved mesophyll conductance. These responses were accompanied by increases in both photosynthesis and respiration rates, without affecting the activity of photosynthetic and respiratory enzymes and the expression of other transporter genes in guard cells, which ultimately led to improved growth. Collectively, our results highlight that the transport of organic acids plays a key role in plant cell metabolism and demonstrate that AtQUAC1 reduce diffusive limitations to photosynthesis, which, at least partially, explain the observed increments in growth under well-watered conditions.

Mitochondrial carriers (MC) are a large family (MCF) of inner membrane transporters displaying diverse, yet often redundant, substrate specificities, as well as differing spatio-temporal patterns of expression; there are even increasing examples of non-mitochondrial subcellular localization. The number of these six trans-membrane domain proteins in sequenced plant genomes ranges from 39 to 141, rendering the size of plant families larger than that found in Saccharomyces cerevisiae and comparable with Homo sapiens. Indeed, comparison of plant MCs with those from these better characterized species has been highly informative. Here, we review the most recent comprehensive studies of plant MCFs, incorporating the torrent of genomic data emanating from next-generation sequencing techniques. As such we present a more current prediction of the substrate specificities of these carriers as well as review the continuing quest to biochemically characterize this feature of the carriers. Taken together, these data provide an important resource to guide direct genetic studies aimed at addressing the relevance of these vital carrier proteins.

Although structurally related, mitochondrial carrier family (MCF) proteins catalyze the specific transport of a range of diverse substrates including nucleotides, amino acids, dicarboxylates, tricarboxylates, cofactors, vitamins, phosphate and H⁺. Despite their name, they do not, however, always localize to the mitochondria, with plasma membrane, peroxisomal, chloroplast and thylakoid and endoplasmic reticulum localizations also being reported. The existence of plastid-specific MCF proteins is suggestive that the evolution of these proteins occurred after the separation of the green lineage. That said, plant-specific MCF proteins are not all plastid-localized, with members also situated at the endoplasmic reticulum and plasma membrane. While by no means yet comprehensive, the in vivo function of a wide range of these transporters is carried out here, and we discuss the employment of genetic variants of the MCF as a means to provide insight into their in vivo function complementary to that obtained from studies following their reconstitution into liposomes.

Lysine represents a metabolic hub linking mitochondrial energy status with amino acid catabolism, yet its role in coordinating plant growth and development remains poorly characterised. The dapat mutant, which is deficient in L,L ‐diaminopimelate aminotransferase (DAPAT), exhibits severe growth inhibition associated with broad metabolic imbalance. This metabolic reprogramming is characterised by simultaneous depletion of carbohydrates (sugars and starch), and organic acids, accompanied by elevated amino acid pools, reflecting a profound disruption of carbon–nitrogen balance. These metabolic constraints coincide with altered expression of gibberellin (GA) biosynthetic genes ( CPS , KS , GA3ox1 ), suggesting a potential link between lysine metabolism, energy status, and GA‐mediated growth regulation. We therefore hypothesised that aberrant developmental defects in dapat arise from impaired GA metabolism. To test this hypothesis, we treated mutant plants with exogenous GA₃. Multivariate metabolomic analysis revealed a striking disconnect: GA restored the normal morphological phenotype of dapat but failed to correct the underlying metabolic dysfunction. GA‐treated dapat plants maintain amino acid remobilisation despite growth restoration, as indicated by pronounced DIN6 induction, a marker of catabolic stress following energy starvation. These findings establish that lysine biosynthesis represents a critical metabolic constraint on plant development, and that growth hormone signalling can decouple morphological rescue from metabolic homoeostasis. This work exposes a fundamental mechanistic uncoupling between hormone‐induced growth and energy balance in lysine‐deficient plants, highlighting the critical role of lysine metabolism in integrating developmental and energetic cues.