Abstract
Chloroplast development and photosynthesis require the proper assembly and turnover of photosynthetic protein complexes. Chloroplasts harbor a repertoire of proteases to facilitate proteostasis and development. We have previously used an Arabidopsis leaf variegation mutant, yellow variegated2 (var2), defective in thylakoid FtsH protease complexes, as a tool to dissect the genetic regulation of chloroplast development. Here, we report a new genetic enhancer mutant of var2, enhancer of variegation3-1 (evr3-1). We confirm that EVR3 encodes a chloroplast metalloprotease, reported previously as ethylene-dependent gravitropism-deficient and yellow-green1 (EGY1)/ammonium overly sensitive1 (AMOS1). We observed that mutations in EVR3/EGY1/AMOS1 cause more severe leaf variegation in var2-5 and synthetic lethality in var2-4 Using a modified blue-native PAGE system, we reveal abnormal accumulations of photosystem I, photosystem II, and light-harvesting antenna complexes in EVR3/EGY1/AMOS1 mutants. Moreover, we discover distinct roles of VAR2 and EVR3/EGY1/AMOS1 in the turnover of photosystem II reaction center under high light stress. In summary, our findings indicate that two chloroplast metalloproteases, VAR2/AtFtsH2 and EVR3/EGY1/AMOS1, function coordinately to regulate chloroplast development and reveal new roles of EVR3/EGY1/AMOS1 in regulating chloroplast proteostasis in Arabidopsis.
Highlights
Chloroplast development and photosynthesis require the proper assembly and turnover of photosynthetic protein complexes
Our findings establish that VAR2/AtFtsH2 and EVR3/ethylene-dependent gravitropism-deficient and yellow-green1 (EGY1)/ammonium overly sensitive1 (AMOS1) coordinate to regulate photosystem II (PSII) stability and chloroplast development
Similar photosystem I (PSI) defects were observed in two other egy1 alleles, egy1–2 and egy1–3 (Fig. S5A). These findings indicate that the abnormal accumulation of PSI complexes in evr3–1 is a direct consequence of the lack of functional EVR3/EGY1/AMOS1
Summary
We have previously used an Arabidopsis leaf variegation mutant, yellow variegated (var2), defective in thylakoid FtsH protease complexes, as a tool to dissect the genetic regulation of chloroplast development. We have identified the SUPPRESSORS OF VARIEGATION (SVRs) loci, which encode many components involved in chloroplast translation and gene expression [24, 28,29,30,31,32,33,34] The disruptions of these SVR genes cause a reduction in plastid gene expression and translation and are sufficient for the suppression of variegation phenotypes, establishing strong genetic and functional relationships between thylakoid FtsH complexes and plastid gene expression. Molecular cloning and complementation confirmed that loss-of-function mutations in EVR3 greatly enhance var leaf variegation, and EVR3 encodes a chloroplast metalloprotease which was previously reported as ethylene-dependent gravitropism-deficient and yellow-green (EGY1) and ammonium overly sensitive (AMOS1) [37, 38]. Our findings establish that VAR2/AtFtsH2 and EVR3/EGY1/AMOS1 coordinate to regulate PSII stability and chloroplast development
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