Search

Using plants as hosts for production of complex, high-value compounds and therapeutic proteins has gained increasing momentum over the past decade. Recent advances in metabolic engineering techniques using synthetic biology have set the stage for production yields to become economically attractive, but more refined design strategies are required to increase product yields without compromising development and growth of the host system. The ability of plant cells to differentiate into various tissues in combination with a high level of cellular compartmentalization represents so far the most unexploited plant-specific resource. Plant cells contain organelles called plastids that retain their own genome, harbour unique biosynthetic pathways and differentiate into distinct plastid types upon environmental and developmental cues. Chloroplasts, the plastid type hosting the photosynthetic processes in green tissues, have proven to be suitable for high yield protein and bio-compound production. Unfortunately, chloroplast manipulation often affects photosynthetic efficiency and therefore plant fitness. In this respect, plastids of non-photosynthetic tissues, which have focused metabolisms for synthesis and storage of particular classes of compounds, might prove more suitable for engineering the production and storage of non-native metabolites without affecting plant fitness. This review provides the current state of knowledge on the molecular mechanisms involved in plastid differentiation and focuses on non-photosynthetic plastids as alternative biotechnological platforms for metabolic engineering.

Optimizal photosynthetic performance requires that equal amounts of light are absorbed by photosystem II (PSII) and photosystem I (PSI), which are functionally linked through the photosynthetic electron transport chain. However, photosynthetic organisms must cope with light conditions that lead to the preferential stimulation of one or other of the photosystems. Plants react to such imbalances by mounting acclimation responses that redistribute excitation energy between photosystems and restore the photosynthetic redox poise. In the short term, this involves the so-called state transition process, which, over periods of minutes, alters the antennal cross-sections of the photosystems through the reversible association of a mobile fraction of light-harvesting complex II (LHCII) with PSI or PSII. Longer-lasting changes in light quality initiate a long-term response (LTR), occurring on a timescale of hours to days, that redresses imbalances in excitation energy by changing the relative amounts of the two photosystems. Despite the differences in their timescales of action, state transitions and LTR are both triggered by the redox state of the plastoquinone (PQ) pool, via the activation of the thylakoid kinase STN7, which appears to act as a common redox sensor and/or signal transducer for both responses. This mini-review highlights recent findings concerning the role of STN7 in coordinating short- and long-term photosynthetic acclimation responses.