Apgr5suppressor screen uncovers a distinct mechanism safeguarding the cytochromeb6fcomplex from damage through PGR5

Abstract

ABSTRACTPROTON GRADIENT REGULATION5 (PGR5) is thought to promote cyclic electron flow (CEF) and its deficiency causes increased photosensitivity of photosystem I (PSI), leading to lethality under fluctuating light (FL). By screening for suppressor mutations that rescue FL lethality ofpgr5plants, we identified a portfolio of mutations affecting 12 photosynthesis-related proteins. Six are required for proper PSII function, one (CcdA) promotes cytochrome (cyt)b6fassembly, and another (PAA1) provides plastocyanin with its copper cofactor. Two other mutations are associated with the chloroplast FBPase cFBP1. This, together with targeted knockout of other genes in thepgr5background, suggests three pathways to restore FL viability: (i) reduced electron flow to PSI due to defects in PSII, cytb6for plastocyanin but not PSI, (ii) increased electron flow from PSI due to inactivation of ACHT2, a regulator of cFBP1 activity, and (iii) hyperactivity of the NDH-dependent CEF due to inactivation of cFBP1. The remaining two suppressor mutations affected the cytb6fcomplex. PFSC1 controls cytb6faccumulation at early developmental stages. DEIP1/NTA1, previously suggested to be essential for cytb6fassembly, appears to protect cytb6ffrom deleterious effects of PGR5, since plants lacking both DEIP1/NTA1 and PGR5 are viable and accumulate cytb6f.