CLPC2 plays specific roles in CLP complex-mediated regulation of growth, photosynthesis, embryogenesis and response to growth-promoting microbial compounds
Authors: Leal-Lopez, J., Bahaji, A., De Diego, N., Tarkowski, P., Baroja-Fernandez, E., Munoz, F. J., Almagro, G., Perez, C. E., Bastidas-Parrado, L. A., Loperfido, D., Caporalli, E., Ezquer, I., Lopez-Serrano, L., Ferez-Gomez, A., Coca-Ruiz, V., Pulido, P., Morcillo, R. J. L., Pozueta-Romero, J.
The study demonstrates that the plastid chaperone CLPC2, but not its paralogue CLPC1, is essential for Arabidopsis responsiveness to microbial volatile compounds and for normal seed and seedling development. Loss of CLPC2 alters the chloroplast proteome, affecting proteins linked to growth, photosynthesis, and embryogenesis, while overexpression of CLPC2 mimics CLPC1 deficiency, highlighting distinct functional roles within the CLP protease complex.
The study examines how ectopic accumulation of methionine in Arabidopsis thaliana leaves, driven by a deregulated AtCGS transgene under a seed‑specific promoter, reshapes metabolism, gene expression, and DNA methylation. High‑methionine lines exhibit increased amino acids and sugars, activation of stress‑hormone pathways, and reduced expression of DNA methyltransferases, while low‑methionine lines show heightened non‑CG methylation without major transcriptional changes. Integrated transcriptomic and methylomic analyses reveal a feedback loop linking sulfur‑carbon metabolism, stress adaptation, and epigenetic regulation.
In a two-year controlled-environment experiment, diploid and tetraploid individuals of wild-type and cultivar Marshall annual ryegrass (Lolium multiflorum) were grown under elevated CO2 (540 vs 800 ppm) and differing evapotranspiration regimes. Elevated CO2 increased total biomass by 44% across ploidy levels, and tetraploid wild-type plants matched the improved cultivar in growth and forage quality, indicating that chromosome manipulation and wild genetic resources can enhance climate resilience.
The study shows that the SnRK1 catalytic subunit KIN10 directs tissue-specific growth‑defense programs in Arabidopsis thaliana by reshaping transcriptomes. kin10 knockout mutants exhibit altered root transcription, reduced root growth, and weakened defense against Pseudomonas syringae, whereas KIN10 overexpression activates shoot defense pathways, increasing ROS and salicylic acid signaling at the cost of growth.