Lund University is celebrating 350 years. Read more on lunduniversity.lu.se

Menu

Javascript is not activated in your browser. This website needs javascript activated to work properly.
You are here

Cell redox control under plant stress

Background: Mitochondrial control of cell redox levels

In plant respiration, carbon compounds are broken down for synthesis of ATP, which provides the energy needed for cellular processes. Carbohydrates and lipids are broken down to organic acids, which mitochondria oxidise while reducing NAD+ to NADH. The NADH is oxidised and the electrons transferred to oxygen by the respiratory chain in the inner mitochondrial membrane. In this process, enzyme complexes pumps protons across the membrane, creating a membrane potential used for the synthesis of ATP. However, plants have enzymes that prevent the conservation of energy. These are called “energy bypasses”, and include external and internal alternative NAD(P)H dehydrogenases (Ndex and Ndin), alternative oxidases (AOX), and uncoupling proteins.

The distribution of redox energy

The distribution of redox energy between plant processes via NADH and NADPH, and how their levels, in turn, may be regulated by the mitochondrial electron transport chain. Cytosolic NADH and NADPH interacts with major growth processes like photosynthesis, nitrogen metabolism and central biosynthetic reactions. NADPH also takes part in reactions important for the plant responses against biotic and abiotic stress (e.g. involving ROS metabolism and signalling).

These proteins allow larger flexibility in energy efficiency and substrate use. Especially, alternative NAD(P)H dehydrogenases can regulate the cellular levels of NADH and NADPH (see Figure). These molecules are the major distributors of redox energy in cells, and interact with many processes active in the central and intermediate carbon metabolism and in responses to plant stress.

Experimental approaches

We follow expression of energy bypass genes, relative to other genes, under variable growth conditions and stressful challenges. One example is a collaborative effort to understand the molecular impact of switches in nitrogen nutrition, and associated pH changes.

By modifying genes for the mitochondrial NAD(P)H dehydrogenases we can influence the whole cell NAD(P)H levels, and directly assess how the cellular NAD(P)H pools control other processes. We have correlated transgenically induced changes in cellular NAD(P)(H) levels to changes in development. We now investigate redox responses to the environment, in particular NAD(P)H-mediated defences enabling plants to cope with biotic and abiotic stress. A particular interest is to analyse if energy bypasses counteract metabolic fluctuations induced by external stress.

Page Manager:
Callos

People involved