Research project The project aims to determine 1) The mechanism behind the regulation of the repressive GUN1-mediated retrograde signal in the plastids 2) How this retrograde signal is transduced from the plastids through the cytosol to the nucleus to control photosynthetic gene expression 3) The nuclear regulatory component(s) responsible for the major chromatin changes associated with the increase in nuclear photosynthetic gene expression in response to loss of the repressive GUN1-mediated retrograde signal.
The project is financed by the Swedish research Council.
The presence of genes encoding organellar proteins in both the nucleus and the different organelles necessitates tight coordination of expression by the different genomes. The photosynthetic machinery in the chloroplast, for example, is built using proteins encoded both in the nucleus and plastids. In the photosynthetic electron transport complexes of the thylakoid membrane, the core subunits are encoded by the plastid genome and the peripheral subunits are encoded by the nuclear genome. In the stroma, the large subunit of RUBISCO is encoded by the plastid, whereas the small subunit is nuclear encoded. To ensure that all these photosynthetic complexes are assembled stoichiometrically, and to enable their rapid reorganization in response to a changing environment, the activities of the nuclear and chloroplast genomes must be closely coordinated through intracellular signalling, including both anterograde and retrograde controls. Anterograde mechanisms (nucleus-to-organelle) coordinate gene expression in the organelles with cellular and environmental cues that are perceived and choreographed by genes in the nucleus. This type of traffic includes nuclear encoded proteins that regulate the transcription and translation of organellar genes. Retrograde (organelle-to-nucleus) signalling, on the other hand, coordinates the expression of nuclear genes encoding organellar proteins with the metabolic and developmental state of the plastid.
Mitochondria and chloroplasts are the powerhouses of the cell and exposure to stress inhibits metabolic activities leading to severe constraints on cellular energy homeostasis. Failure to restore either respiration or photosynthesis severely affects vigour, and possibly survival, of the organism. Retrograde signalling networks are essential for the establishment of cellular energy metabolism as well as recovery of energy metabolism following stress. Failures in this communication system lead to dysfunctional organelles and to the collapse of cellular energy metabolism. For plants this can have fatal consequences, and in humans dysfunctional mitochondria have been linked to the aging process and to several severe diseases. The overall goal of my research is to understand the regulation and control of cellular energy metabolism. In this project I focus on the intracellular signalling network controlling the development of functional chloroplasts and thereby the establishment of photosynthetic activity. This developmental process drives a cellular shift from requiring external energy sources for growth and development to becoming a supplier of energy to support growth of new developing tissues. This transition in cellular metabolic activity requires a complex regulatory network involving several cellular compartments, extensive chromatin reorganisation and massive transcriptional changes.