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Iron deficiency-mediated stress regulation of four subgroup Ib BHLH genes in Arabidopsis thaliana

机译:铁缺乏介导的拟南芥四个亚型Ib BHLH基因的胁迫调控

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摘要

Networks of transcription factors control physiological, developmental and environmental responses. Root iron acquisition responses are controlled by the essential bHLH protein FIT. Recently, two group Ib BHLH genes were reported to be iron deficiency-regulated. Here, we studied expression patterns of these two group Ib BHLH genes and of their two closest homologs to analyze whether their regulation would support a function in iron deficiency responses. We found that BHLH038, BHLH039, BHLH100 and BHLH101 (comprising a subgroup of BHLH Ib genes) were up regulated by iron deficiency in roots and leaves. Single insertion mutants had no visible phenotype and were capable of inducing root iron acquisition responses, presumably due to functional redundancy. Specific metal treatments like nickel, high zinc or high copper resulted in induction of the four BHLH Ib genes whereas high iron, low copper and low zinc repressed gene expression. Induction of the four BHLH Ib genes was also found in multiple iron acquisition mutants including fit. Ectopic activation of FIT did not suppress the four BHLH Ib genes. Split-root analyses using promoter-GUS lines showed that FIT and BHLH100 promoters were controlled by different local and systemic signals involved in their regulation by iron. These results indicated that the four BHLH Ib genes were induced independently from FIT by conditions causing iron deficiency. Taken together, BHLH038, BHLH039, BHLH100 and BHLH101 function differently from FIT and may be involved in mediating a signal related to iron deficiency-induced stress and/or internal iron homeostasis.
机译:转录因子网络控制生理,发育和环境反应。根铁的获取反应受必需的bHLH蛋白FIT控制。最近,据报道有两个Ib BHLH基因被铁缺乏调节。在这里,我们研究了这两组Ib BHLH基因及其两个最接近的同源物的表达模式,以分析它们的调控是否支持铁缺乏反应中的功能。我们发现,BHLH038,BHLH039,BHLH100和BHLH101(包含BHLH Ib基因的一个亚组)受根和叶中铁缺乏的上调。单插入突变体没有可见的表型,并且能够诱导根铁获得应答,大概是由于功能冗余。诸如镍,高锌或高铜的特定金属处理导致了四个BHLH Ib基因的诱导,而高铁,低铜和低锌抑制了基因表达。在包括fit在内的多个铁捕获突变体中也发现了四个BHLH Ib基因的诱导。 FIT的异位激活没有抑制四个BHLH Ib基因。使用启动子-GUS系进行的开根分析表明,FIT和BHLH100启动子受铁调节其参与的不同局部和全身信号的控制。这些结果表明四个BHLH Ib基因是由引起铁缺乏的条件独立于FIT诱导的。综上所述,BHLH038,BHLH039,BHLH100和BHLH101的功能与FIT不同,并且可能参与介导与铁缺乏引起的应激和/或内部铁稳态有关的信号。

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