Genetic Dissection of Organellar-Gene-Expression (OGE)-Dependent Retrograde Signaling in Arabidopsis

拟南芥细胞器基因表达 (OGE) 依赖性逆行信号转导的遗传解析

• 批准号: 42287633
• 负责人: Professor Dr. Dario Leister
• 金额: --
• 依托单位: Lehrstuhl für Molekularbiologie der Pflanzen
• 依托单位国家: 德国
• 项目类别: Research Units
• 财政年份: 2007
• 资助国家: 德国
• 起止时间: 2006-12-31 至 2017-12-31
• 项目状态: 已结题
• 来源: https://gepris.dfg.de/gepris/projekt/42287633?language=en
• 关键词: Genetic; Dissection; Organellar; Gene; Expression

Most plastid proteins are nucleus-encoded and their transcriptional regulation involves retrograde signaling. Impairment of organellar gene expression (OGE) by chemicals such as lincomycin, or mutations such as prpl11 or prors1, trigger a retrograde signaling pathway and result in transcriptional down-regulation of nuclear photosynthetic genes. Work on the Arabidopsis prors1 mutant showed that when OGE is perturbed, signals derived from both chloroplasts and mitochondria cooperate in down regulating nuclear photosynthetic gene expression. In the previous funding period we have generated lines with repressible OGE, discovered that the gun1 mutation overrides OGE signaling triggered by prors1, and identified the first rls (relaxed LHCB repression) mutants with derepressed LHCB expression in the prors1 background. In the next funding period we will identify target genes of OGE and GUN1 signaling starting from transcriptome kinetics of lines with repressible OGE or GUN1 activity. We will classify and characterize the rls mutants and identify at least two RLS genes. Thirdly, we will characterize in detail the role of GUN1 in OGE signaling, considering the possibility that GUN1 functionally interacts with plastid ribosomes. This combined strategy will enable us to identify factors involved in chloroplast or mitochondrial signaling, as well as factors that integrate the activities of the two signaling pathways.

大多数质体蛋白是核编码的，它们的转录调控涉及逆行信号。林可霉素等化学物质或prpl11或pros1等突变对细胞器基因表达（OGE）的损害会触发逆行信号通路，并导致核光合基因的转录下调。对拟南芥突变体pros1的研究表明，当OGE受到干扰时，来自叶绿体和线粒体的信号共同下调核光合基因的表达。在之前的资助期内，我们已经生成了具有可抑制OGE的细胞系，发现gun1突变覆盖了由pros1触发的OGE信号，并在pros1背景下鉴定了第一批LHCB表达降低的rls（松弛LHCB抑制）突变体。在下一个资助期，我们将从OGE或GUN1活性可抑制的细胞系的转录组动力学开始，确定OGE和GUN1信号传导的靶基因。我们将对rls突变体进行分类和表征，并确定至少两个rls基因。第三，考虑到GUN1与质体核糖体功能相互作用的可能性，我们将详细描述GUN1在OGE信号传导中的作用。这种联合策略将使我们能够识别参与叶绿体或线粒体信号传导的因素，以及整合两种信号通路活动的因素。