Williams-Carrier Rosalind, Chotewutmontri Prakitchai, Perkel Sarah, Rojas Margarita, Belcher Susan, Barkan Alice
Institute of Molecular Biology, University of Oregon, Eugene, OR 97405, USA.
Plant Cell. 2025 Apr 2;37(4). doi: 10.1093/plcell/koaf047.
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.
光系统II的D1亚基易受光氧化损伤。光损伤的D1必须被新生的D1取代，以维持光合作用。在植物叶绿体中，D1光损伤通过调节编码D1的psbA mRNA上的翻译起始来调控D1的合成，但其潜在机制尚不清楚。对转质体烟草（Nicotiana tabacum）中报告基因构建体的分析表明，psbA翻译调节因子HCF173通过psbA 5'-UTR中的顺式元件激活。然而，psbA UTR不足以编程光调节的翻译。相反，psbA开放阅读框在顺式中抑制翻译起始，而D1光损伤缓解了这种抑制。HCF173在黑暗中仍与psbA 5'-UTR结合，HCF173的截短可防止黑暗中的抑制，这表明HCF173是抑制的介导因子。我们提出了一个模型来解释这些以及先前的观察结果，该模型是由复合物I组装因子CIA30/NDUFAF1的结构所启发的。我们推测，D1光损伤缓解了新生D1与HCF173的CIA30结构域之间的抑制性共翻译相互作用，光系统II组装因子HCF136促进了这种抑制性相互作用，并且这些事件使HCF173在psbA mRNA上的激活和抑制构象之间切换。这些发现阐明了一种翻译变阻器，可根据不断变化的光照条件优化光合作用。
