Table S1.

Summary of redox homeostasis-deficient mutants used in Fig. 1

Name	Gene identifier	Type of mutation	Biological pathway affected	Ref.
tAPX (thylakoidal ascorbate peroxidase)	AT1G77490	amiRNA-knockdown	Detoxification of H2O2 in the chloroplast thylakoid and detoxification of superoxide by superoxide dismutase in water–water cycle at photosystem I (PSI).	1
sAPX (stromal ascorbate peroxidase)	AT4G08390	T-DNA insertion, homozygous	Detoxification of H2O2 in the chloroplast stroma, where AtSAL1 is also located.	1
phs1 (photosensitive 1)	AT3G47390	T-DNA insertion, homozygous	Involved in riboflavin and FAD synthesis. Mutant allele has increased oxidative stress due to reduced NADPH/NADP+ ratios and overproduction of ROS at PSI under high light.	53
cos1 (coronatine insensitive1 suppresor)	AT2G44050	T-DNA insertion, heterozygous	Involved in the same metabolic pathway as phs1 (riboflavin and FAD synthesis).	59
rax1-1 (regulator of ascorbate peroxidase 2 1-1)	AT4G23100	Point mutation, homozygous	Rate-limiting step of glutathione synthesis. GSH:GSSG redox ratio may be altered under oxidative stress.	54
ntrc (NAPDH-dependent thioredoxin reductase C)	AT2G41680	T-DNA insertion, homozygous	Reduction of 2-Cys peroxiredoxins and redox control within the chloroplast. Deficiency causes hypersensitivity to abiotic stress.	52

Loss-of-function mutants deficient in various aspects of redox homeostasis in the chloroplast were chosen for analysis of AtSAL1 activity under abiotic stress. The mutants are deficient in ROS detoxification, redox control at PSI, or chloroplast redox buffer pathways.