High CO₂ facilitates fatty acid biosynthesis and mitigates cellular oxidative stress caused by CAC2 dysfunction in...

Increasing concentration of CO₂ has significant impacts on many biological processes in plants, and its impact is closely associated with changes in the ratio of photosynthesis to photorespiration. Studies have reported that high CO₂ can promote carbon fixing and alleviate plant oxidative damage in response to environmental stresses. However, the effect of high CO₂ on fatty acid (FA) metabolism and cellular redox balance in FA-deficient plants is rarely reported. In this study, we identified a high-CO₂ -requiring mutant cac2 through forward genetic screening. CAC2 encodes biotin carboxylase, which is one of the subunits of plastid acetyl-CoA carboxylase and participates in de novo FA biosynthesis. Null mutation of CAC2 is embryonic lethal. A point mutation of CAC2 in cac2 mutants produces severe defects in chloroplast development, plant growth and photosynthetic performance. These morphological and physiological defects were largely absent under high CO₂ conditions. Metabolite analyses showed that FA contents in cac2-1 leaves were decreased, while photorespiratory metabolites, such as glycine and glycolate, did not significantly change. Meanwhile, cac2 exhibited higher reactive oxygen species (ROS) levels and mRNA expression of stress-responsive genes than the wild-type, indicating that cac2 plants may suffer oxidative stress under ambient CO₂ conditions. Elevated CO₂ significantly increased FA contents, especially C18:3-FA, and reduced ROS accumulation in cac2-1 leaves. We propose that stress mitigation by high CO₂ in cac2 could be due to increased FA levels by promoting carbon assimilation, and the prevention of over-reduction due to decreased photorespiration.