莱茵衣藻铜反应调节因子1转录因子调控基因的鉴定

Xiaoqing Sun, Matthew LaVoie, Paul A Lefebvre, Sean D Gallaher, Anne G Glaesener, Daniela Strenkert, Radhika Mehta, Sabeeha S Merchant, Carolyn D Silflow
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摘要

氧阻止衣藻(莱茵衣藻)产生氢,部分原因是通过抑制氢化酶基因的转录。我们开发了一种在常氧环境下显示铁氢化酶1 (HYDA1)转录本组成性积累的突变体筛选方法。在HYDA1启动子的控制下,纤毛运动所需的报告基因仅在缺氧时才具有运动性。通过选择即使在常氧环境下也能游泳的突变体,我们获得了组成性表达报告基因的菌株。其中一个已鉴定的突变体影响了编码F-box蛋白3 (FBXO3)的基因,该基因在其他真核生物中参与泛素化和蛋白酶体降解途径。转录组分析显示,该突变名为cehc1-1(氢化酶和铜反应基因的组成表达),可触发铜反应调节因子1 (copper response regulator 1, CRR1)靶标基因的上调。CRR1是一种参与营养铜信号通路和缺氧反应通路的转录因子。CRR1是在缺氧条件下上调HYDA1报告基因表达以及在cehc1-1突变细胞中报告基因组成表达所必需的。CRR1蛋白通常在cu补充细胞中降解,在CEHC1 -1细胞中稳定,支持CEHC1促进CRR1降解的结论。我们的研究结果描述了一种以前未知的CRR1抑制途径,以及可能导致复杂代谢变化的其他途径。
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Identification of a gene controlling levels of the copper response regulator 1 transcription factor in Chlamydomonas reinhardtii
Oxygen prevents hydrogen production in Chlamydomonas (Chlamydomonas reinhardtii), in part by inhibiting the transcription of hydrogenase genes. We developed a screen for mutants showing constitutive accumulation of iron hydrogenase 1 (HYDA1) transcripts in normoxia. A reporter gene required for ciliary motility placed under the control of the HYDA1 promoter conferred motility only in hypoxia. By selecting for mutants able to swim even in normoxia, we obtained strains that constitutively express the reporter gene. One identified mutant was affected in a gene encoding an F-box protein 3 (FBXO3) that participates in ubiquitylation and proteasomal degradation pathways in other eukaryotes. Transcriptome profiles revealed that the mutation, termed cehc1-1 (constitutive expression of hydrogenases and copper-responsive genes), triggers the upregulation of genes known to be targets of copper response regulator 1 (CRR1), a transcription factor involved in the nutritional copper signaling pathway and in the hypoxia response pathway. CRR1 was required for upregulating the HYDA1 reporter gene expression in response to hypoxia and for the constitutive expression of the reporter gene in cehc1-1 mutant cells. The CRR1 protein, normally degraded in Cu-supplemented cells, was stabilized in cehc1-1 cells, supporting the conclusion that CEHC1 facilitates CRR1 degradation. Our results describe a previously unknown pathway for CRR1 inhibition and possibly other pathways leading to complex metabolic changes.
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