Department of Genetics and Bioengineering, Faculty of Engineering, İzmir University of Economics, Sakarya Cad., No: 156, Balcova, 35330, İzmir, Turkey.
Department of Agricultural Genetic Engineering, Ayhan Sahenk Faculty of Agricultural Sciences and Technologies, Ömer Halisdemir University, Merkez, 51240, Nigde, Turkey.
Biometals. 2017 Oct;30(5):685-698. doi: 10.1007/s10534-017-0036-8. Epub 2017 Jul 25.
In plant cells, either excess or insufficient iron (Fe) concentration triggers stress responses, therefore it is strictly controlled. Proteasome-mediated degradation through ubiquitination of Fe homeostasis proteins has just become the focus of research in recent years. Deactivating ubiquitin ligases, COP9 signalosome has a central importance in the translational control of various stress responses. The aim of the study was to investigate COP9 signalosome in Fe deficiency response of Strategy I plants. In silico analysis of a set of Fe-deficiency-responsive genes was conducted against the transcriptome of Arabidopsis csn mutant lines using Genevestigator software. Induced and suppressed genes were clustered in a hierarchical way and gene ontology enrichment categories were identified. In wild-type Arabidopsis, CSN genes did not respond to iron deficiency. In csn mutant lines, under Fe-sufficient conditions, hundreds of Fe-deficiency-responsive genes were misregulated. Among the ones previously characterized for their physiological roles under Fe deficiency IRT1, NAS4, BTS, NRAMP1 were down-regulated while AHA2, MTP8, FRD3 were up-regulated. Unexpectedly, from those which were regulated in opposite ways, some had been repeatedly shown to be tightly co-regulated by the same transcription factor, FIT. Two proteins from DELLA family, which were reported to interact with FIT to repress its downstream, were found to be strikingly repressed in csn mutants. Overall, the study underlined that the absence of a functional CSN greatly impacted the regulation of Fe homeostasis-related genes, in a manner which cannot be explained simply by the induction of the master transcription factor, FIT. Correct expression of Fe deficiency-responsive genes requires an intact COP9 signalosome in Arabidopsis.
在植物细胞中，铁（Fe）浓度过高或过低都会引发应激反应，因此铁浓度受到严格控制。近年来，通过泛素化铁稳态蛋白的蛋白酶体介导降解成为研究的焦点。COPI 信号体作为一种去泛素化酶，在各种应激反应的翻译调控中具有核心重要性。本研究旨在探讨 COPI 信号体在策略 I 植物缺铁反应中的作用。使用 Genevestigator 软件，对拟南芥 csn 突变体系的转录组进行铁缺乏响应一组基因的计算机分析。采用层次聚类的方法对诱导和抑制基因进行聚类，并鉴定基因本体富集类别。在野生型拟南芥中，CSN 基因对缺铁没有反应。在 csn 突变体系中，在铁充足的条件下，数百个缺铁响应基因被错误调控。在以前被认为在缺铁条件下具有生理作用的基因中，IRT1、NAS4、BTS、NRAMP1 下调，而 AHA2、MTP8、FRD3 上调。出乎意料的是，在那些以相反方式被调控的基因中，有些基因被同一个转录因子 FIT 紧密地共同调控。两种来自 DELLA 家族的蛋白质，据报道与 FIT 相互作用以抑制其下游基因的表达，在 csn 突变体中被显著抑制。总的来说，该研究强调，缺乏功能正常的 CSN 会极大地影响与铁稳态相关基因的调控，其方式不能简单地归因于主转录因子 FIT 的诱导。拟南芥中缺铁响应基因的正确表达需要一个完整的 COPI 信号体。
