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The D1 subunit of photosystem II (PSII) is subject to light-induced damage. In plants, D1 photodamage activates translation of chloroplastpsbAmRNA encoding D1, providing D1 for PSII repair. Three D1 assembly factors have been implicated in the regulatory mechanism: HCF244 and RBD1 activatepsbAtranslation, whereas HCF136 repressespsbAtranslation in the dark. To clarify the regulatory circuit, we analyzedpsbAribosome occupancy in dark-adapted and illuminatedrbd1andrbd1;hcf136double mutants in Arabidopsis and in Zm-hcf244and Zm-hcf244;Zm-hcf136double mutants in maize. The results show that RBD1 is required for light-inducedpsbAtranslation but has only a small effect onpsbAribosome occupancy in the dark. RBD1 is not required forpsbAtranslation when HCF136 is absent, indicating that RBD1 activatespsbAtranslation in the light by inhibiting HCF136’s repressive effect. By contrast, HCF244 is required to recruit ribosomes topsbAmRNA in light, dark, and in the absence of HCF136. We demonstrate further that HCF244 is not required for the translational activator HCF173 to bind thepsbA5’UTR. These results show that RBD1 is central to the perception of the D1 photodamage that triggers D1 synthesis and that it activatespsbAtranslation by relieving repression by an HCF136-dependent assembly intermediate. HCF244 activates downstream of those events without impacting HCF173’s binding topsbAmRNA. The results implicate a feature of nascent D1 that is affected by both HCF136 and RBD1 as the signal that reports D1 photodamage to regulatepsbAtranslation rate as needed for PSII repair.