ArticleThe Plant cell2025
The psbA open reading frame acts in cis to toggle HCF173 from an activator to a repressor for light-regulated psbA translation in plants.
Article in The Plant cell, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
What it found
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Who cites it
5 citing papers in PubMed.
- Conserved DNA architect couples chloroplast development to cell cycle in developing cotyledons.Nature plants · 2026Article
- Characterization and evolutionary insights into complete mitochondrial genome ofFrontiers in plant science · 2026Article
- Effects of light on chloroplast translation in Marchantia polymorpha are similar to those in angiosperms and are not influenced by light-independent chlorophyll synthesis.The Plant journal : for cell and molecular biology · 2025Article
- Assembly-dependent translational feedback regulation of photosynthetic proteins in land plants.Nature plants · 2025Article
- Opposing action of photosystem II assembly factors RBD1 and HCF136 underlies light-regulatedProceedings of the National Academy of Sciences of the United States of America · 2025Article
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Authors and funding
6 authors.
Funding
Abstract
The D1 subunit of photosystem II is subject to photooxidative damage. Photodamaged D1 must be replaced with nascent D1 to maintain photosynthesis. In plant chloroplasts, D1 photodamage regulates D1 synthesis by modulating translation initiation on psbA mRNA encoding D1, but the underlying mechanisms are unknown. Analyses of reporter constructs in transplastomic tobacco (Nicotiana tabacum) showed that the psbA translational regulator HCF173 activates via a cis-element in the psbA 5'-UTR. However, the psbA UTRs are not sufficient to program light-regulated translation. Instead, the psbA open reading frame represses translation initiation in cis, and D1 photodamage relieves this repression. HCF173 remains bound to the psbA 5'-UTR in the dark and truncation of HCF173 prevents repression in the dark, implicating HCF173 as a mediator of repression. We propose a model that accounts for these and prior observations, which is informed by structures of the Complex I assembly factor CIA30/NDUFAF1. We posit that D1 photodamage relieves a repressive cotranslational interaction between nascent D1 and HCF173's CIA30 domain, that the photosystem II assembly factor HCF136 promotes this repressive interaction, and that these events toggle HCF173 between activating and repressive conformations on psbA mRNA. These findings elucidate a translational rheostat that optimizes photosynthesis in response to shifting light conditions.
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