Abstract
Perturbations in organellar gene expression (OGE) and the thylakoid redox state (TRS) activate retrograde signaling pathways that adaptively modify nuclear gene expression (NGE), according to developmental and metabolic needs. The prors1-1 mutation in Arabidopsis down-regulates the expression of the nuclear gene Prolyl-tRNA Synthetase1 (PRORS1) which acts in both plastids and mitochondria, thereby impairing protein synthesis in both organelles and triggering OGE-dependent retrograde signaling. Because the mutation also affects thylakoid electron transport, TRS-dependent signals may likewise have an impact on the changes in NGE observed in this genotype. In this study, we have investigated whether signals related to TRS are actually integrated into the OGE-dependent retrograde signaling pathway. To this end, the chaos mutation (for chlorophyll a/b binding protein harvesting-organelle specific), which shows a partial loss of PSII antennae proteins and thus a reduction in PSII light absorption capability, was introduced into the prors1-1 mutant background. The resulting double mutant displayed a prors1-1-like reduction in plastid translation rate and a chaos-like decrease in PSII antenna size, whereas the hyper-reduction of the thylakoid electron transport chain, caused by the prors1-1 mutation, was alleviated, as determined by monitoring chlorophyll (Chl) fluorescence and thylakoid phosphorylation. Interestingly, a substantial fraction of the nucleus-encoded photosynthesis genes down-regulated in the prors1-1 mutant are expressed at nearly wild-type rates in prors1-1 chaos leaves, and this recovery is reflected in the steady-state levels of their protein products in the chloroplast. We therefore conclude that signals related to photosynthetic electron transport and TRS, and indirectly to carbohydrate metabolism and energy balance, are indeed fed into the OGE-dependent retrograde pathway to modulate NGE and adjust the abundance of chloroplast proteins.
Highlights
Several features link mitochondria and plastids within the plant cell
We have investigated the extent to which signals related to photosynthetic electron transport contribute to the organellar gene expression (OGE)-dependent retrograde signaling pathway, by introducing the chaos mutation (Klimyuk et al, 1999) into the prors1-1 mutant background
In agreement with these observations, a decrease in the degree of reduction of QA and the plastoquinone (PQ) pool was observed in chaos and prors1-1 chaos leaves (Figure 2D), suggesting a reduced net electron injection into the thylakoid transport chain, caused by chaos mutation
Summary
Several features link mitochondria and plastids within the plant cell. Both organelles maintain and express genetic information, conduct electron transport functions, and are metabolically interdependent (Woodson and Chory, 2008).In addition, the majority of mitochondrial and plastid proteins are nucleus-encoded (Kleine et al, 2009a). Several features link mitochondria and plastids within the plant cell. Both organelles maintain and express genetic information, conduct electron transport functions, and are metabolically interdependent (Woodson and Chory, 2008). (1) Biogenic control, i.e., developmental control of organelle biogenesis needs to be appropriately staged and the required subunits and cofactors need to be present in correct stoichiometry for accurate assembly; and (2) operational control, representing rapid adjustments that are made to energy metabolism in response to environmental and developmental constraints to maintain optimal production and both limit and repair damage induced by oxidative stress (reviewed in Leister, 2005; Pesaresi et al, 2007; Pogson et al, 2008; Woodson and Chory, 2008; Barajas-Lopez et al, in press). Given the complexity of organellar functions, a variety of interlinked retrograde pathways can be expected (Kleine et al, 2009b; Leister, 2012)
Sign-in/Register to view highlights & summary Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
