Department of Biological Sciences, Royal Holloway University of London, Egham TW20 0EX, UK.
Department of Plant Sciences, University of Oxford, South Parks Road, Oxford OX1 3RB, UK.
Philos Trans R Soc Lond B Biol Sci. 2020 Jun 22;375(1801):20190400. doi: 10.1098/rstb.2019.0400. Epub 2020 May 4.
Defects in chloroplast development are 'retrograde-signalled' to the nucleus, reducing synthesis of photosynthetic or related proteins. The mutant manifests virescence, a slow-greening phenotype, and is defective at an early stage in plastid development. Greening cotyledons or early leaf cells of exhibit immature chloroplasts which fail to fill the available cellular space. Such chloroplasts show reduced expression of genes of photosynthetic function, dependent on the plastid-encoded polymerase (PEP), while the expression of genes of housekeeping function driven by the nucleus-encoded polymerase (NEP) is elevated, a phenotype shared with mutants in plastid genetic functions. We attribute this phenotype to reduced expression of specific PEP-controlling sigma factors, elevated expression of (NEP) genes and maintained replication of plastid genomes (resulting in densely coalesced nucleoids in the mutant), i.e. it is due to an anterograde nucleus-to-chloroplast correction, analogous to retention of a juvenile plastid state. Mutants in plastid protein import components, particularly those involved in housekeeping protein import, also show this 'retro-anterograde' correction. Loss of CUE8 also causes changes in mRNA editing. The overall response has strong fitness value: loss of GUN1, an integrator of retrograde signalling, abolishes elements of it (albeit not others, including editing changes), causing bleaching and eventual seedling lethality upon . This highlights the adaptive significance of virescence and retrograde signalling. This article is part of the theme issue 'Retrograde signalling from endosymbiotic organelles'.
叶绿体发育缺陷会向细胞核发出“逆行信号”，从而减少光合作用或相关蛋白的合成。突变体表现出返祖绿化现象，即缓慢变绿的表型，并且在质体发育的早期阶段存在缺陷。突变体的绿色子叶或早期叶片细胞表现出不成熟的叶绿体，无法填满可用的细胞空间。这些叶绿体表现出依赖于质体编码聚合酶（PEP）的光合作用功能基因表达减少，而由核编码聚合酶（NEP）驱动的管家功能基因表达升高，这一表型与质体遗传功能突变体共享。我们将这种表型归因于特定 PEP 控制 σ 因子表达减少、 （NEP）基因表达升高以及质体基因组复制的维持（导致突变体中核点密集凝聚），即它是由于前向核质体校正，类似于保留幼年质体状态。质体蛋白输入组件的突变体，特别是那些参与管家蛋白输入的突变体，也表现出这种“逆行前向”校正。CUE8 的缺失也会导致 mRNA 编辑的改变。总体反应具有很强的适应价值：逆行信号整合子 GUN1 的缺失会消除其部分功能（尽管不是其他功能，包括编辑变化），导致白化病，并最终在 下使幼苗致死。这凸显了返祖绿化和逆行信号的适应性意义。本文是“来自共生细胞器的逆行信号”主题问题的一部分。
