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Our research

Plant metabolism owns an extraordinary plasticity, which reflects plant adaptations to ever changing environmental conditions.

Our research is dedicated to:

  • unraveling regulatory processes that coordinate plant metabolic pathways in dependence on developmental and environmental cues
  • understanding the evolution, regulation, and biological implications of small molecule damage control systems


Plant metabolism, just like that of other organisms, extends beyond the limits of central pathways and is also prone to errors. Small molecules such as coenzymes, cofactors, metabolic intermediates, and inorganic molecules can be damaged through the side activity of promiscuous enzymes or through spontaneous reactions. The resulting metabolic products – damaged molecules – are in the best case useless but in most cases harmful to the cell.
The formation of these unwanted compounds is boosted when plants are exposed to abiotic stresses such as high light intensities, salinity, and drought.


Plants evolved at least three distinct systems to control small molecule damage: (i) repair, (ii) scavenging, and (iii) steering.

(i)    Repair systems return a damaged metabolite to its original state via one or more enzymatic reactions (metabolite proofreading).

-      An illustrative example of a one-step repair system we are working on is L-2-hydroxyglutarate dehydrogenase. This enzyme eliminates L-2-hydroxyglutarate, a metabolite abnormally produced by mitochondrial malate dehydrogenase activity.

-      We also extensively work on the photorespiratory pathway. This is a multiple-step repair system that recovers carbon diverted to 2-phosphoglycolate, a dead-end metabolic product of high toxicity produced by the oxygenase side activity of Rubisco.


(ii)   Scavenging systems convert reactive metabolites to harmless products. Research in my group focuses on diverse aspects of important scavenging mechanisms.

-    One mechanism we study is the glyoxalase system, which converts reactive carbonyl species into metabolic intermediates such as glycolate or D-lactate.


-    Another studied process is the action of different scavenging systems for the maintenance of reactive oxygen species at levels that allow them to act as cellular messengers while at the same time preventing oxidative stress.




  (iii)    Steering systems evolved to by-pass the production of damaged small molecules. A mechanism involved is the reduction of the unwanted side reaction of an enzyme by changing the supply of the substrates for that reaction.

 -       One such mechanism in which we are working on is the C4 photosynthetic pathway. This CO2-concentrating pump evolved as a mechanism to reduce the production of toxic 2-phosphoglycolate by the oxygenase activity of Rubisco.





Current research projects


Cellular signaling through reactive oxygen species

During photosynthesis, the chloroplasts and the peroxisomes are the main sources of reactive oxygen species, especially of hydrogen peroxide (H2O2). H2O2 causes oxidative damage, but also acts in signaling. A major aim of my research is to dissect the genetic networks that are involved in H2O2 signaling and to assess specific and common responses towards H2O2 signaling after its production in different subcellular compartments. Using a non-invasive approach to modulate the metabolic production of H2O2 in A. thaliana chloroplasts, we showed that a moderate production of H2O2 from chloroplasts or peroxisomes induces two types of responses: Chloroplast-produced H2O2 has crucial sensory and signaling functions, while peroxisome-produced H2O2 most likely induces stress tolerance responses.


Detoxification of reactive carbonyl species

Reactive carbonyl species (RCS) such as methylglyoxal and glyoxal are highly reactive toward different cellular macromolecules. The primary source of these RCS is the glycolytic pathway. However, as a unique feature of plant cells, the activity of the Calvin Benson cycle results in a second source of RCS. Ongoing work in our group indicates that the individual components of the system are active at specific plant developmental stages and metabolic conditions induced by cellular and environmental changes. The involvement of different organelles during the detoxification of methylglyoxal implies a synchronization of the corresponding enzymatic and transport activities between the cellular compartments.


Molecular evolution of enzymes involved in the C4 photosynthetic pathway

All species that evolved C4 photosynthesis as a pre-emptive pathway for the suppression of the oxygenase side activity of Rubisco have co-opted malate as a key metabolite in this process. Despite the complexity of C4 photosynthesis, this pre-emptive mechanism constitutes a striking example of convergent evolution: it has evolved independently in more than 60 angiosperm lineages. Importantly, all enzymes required for C4 photosynthesis have orthologs in C3 species, where they perform other functions. In the evolution of C4 biochemistry, these enzymes required concerted changes in their cell type-specific gene expression as well as adjustments of their structural and kinetic properties. Research in my group centers on the mechanisms behind the evolution of C4 decarboxylases.

Photorespiration and glycolate metabolism

During photorespiration, dephosphorylation of 2-phosphoglycolate in the chloroplasts produces glycolate. Even minute traces of these metabolites exert cumulative detrimental effects. Enzymatic removal of glycolate is an essential part of photorespiration and is catalyzed by two phylogenetically unrelated enzymes. In cyanobacteria and green algae of the chlorophyta lineage, glycolate oxidation is catalyzed by glycolate dehydrogenase (GlcDH). In contrast, green algae of the Charophyceae lineage and land plants use glycolate oxidase (GOX) activity, which produces H2O2 in peroxisomes. We recently clarified the evolution of GOX and discovered that GOX and GlcDH activities never co-exist in an organism. Currently, we elucidate the composition of the photorespiratory pathway in algae that arose through secondary endosymbioses and we analyze glycolate metabolism in non-photosynthetic tissues.

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