Fig. 7: A proposed model of albino formation mediated by ospus1 under low temperature.

(Left) In wild-type 9311, PUS1 is upregulated and catalyzes the pseudouridylation of pre-rRNAs under cold conditions, enabling normal chloroplast ribosome assembly and translation, thus maintaining homeostasis in chloroplast metabolism. (Middle) A deficiency in chloroplast pre-rRNA pseudouridylation in ospus1 mutants results in aberrant chloroplast ribosomes and defects in plastid translation, which then leads to an imbalance of chloroplast metabolism. The disruption of chloroplast homeostasis generated a chemical/signal that was transmitted into mitochondrion and induced O2•- overproduction from the mitochondrial ETC (mETC) complex I. The mitochondrial O2•- then caused the albino phenotype in ospus1 under low temperatures, by oxidizing target proteins (Oxi-PTMs), which remain to be identified. (Right) Mutations in a mitochondrial PPR protein (SOP10) that directly binds to nad4 and nad5 transcripts and regulates splicing of their first exons, decreases mETC complex I capacity and O2•- accumulation, and suppresses the albino phenotype of ospus1, enhances rice cold tolerance in wild-type 9311.