High CO 2 facilitates fatty acid biosynthesis and mitigates cellular oxidative stress caused by CAC2 dysfunction in Arabidopsis.

Increasing concentration of CO 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 CO can promote carbon fixing and alleviate plant oxidative damage in response to environmental stresses. However, the effect of high CO on fatty acid (FA) metabolism and cellular redox balance in FA-deficient plants is rarely reported. In this study, we identified a high-CO -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 CO conditions. Metabolite analyses showed that FA contents in cac2-1 leaves were decreased, while photorespiratory metabolites, such as glycine and glycolate, did not significantly changed. Meanwhile, cac2 exhibited higher ROS levels and mRNA expression of stress-responsive genes than the wild type, indicating that cac2 plants may suffer oxidative stress under ambient CO conditions. Elevated CO significantly increased FA contents, especially C18:3-FA, and reduced ROS accumulation in cac2-1 leaves. We propose that stress mitigation by high CO in cac2 could be due to increased FA levels by promoting carbon assimilation, and the prevention of over-reduction due to decreased photorespiration.