■ILR3和PYE在调节缺铁下GLS积累的调节网络中发挥作用。人们对植物中铁(Fe)稳态与其他代谢过程之间的串扰所涉及的分子过程知之甚少。在拟南芥中,转录因子IAA-LEUCINERESISTANT3(ILR3)调节铁缺乏反应,脂肪族芥子油苷(GLS)的生物合成和病原体反应。还已知ILR3与其同源物相互作用,POPEYE(PYE),这也在Fe反应中起作用。然而,关于ILR3如何调节如此多样化的过程知之甚少,特别是,通过与PYE的互动。由于GLS是作为对抗伤人病原体的防御机制的一部分而产生的,我们检查了pILR3::β-葡萄糖氨酸酶的表达,发现铁缺乏增强了创伤诱导的根中ILR3的表达,并且ILR3是响应创伤病原体而诱导的。甜菜根囊肿线虫(Heteroderaschachtii)。我们还检查了pye-1,ilr3-2和pye-1xilr3-2(pxi)突变体中参与Fe稳态和脂肪族GLS生物合成的基因的表达模式,发现ILR3和PYE差异调节参与这些过程的基因的表达。我们测量了不同Fe条件下的GLS水平和甜菜根囊肿线虫感染率,发现在ilr3-2和pxi突变体中长链GLS水平升高。长链GLS积累的增加与不存在Fe的ilr3-2和pxi突变体中线虫抗性的提高有关。我们的发现表明,ILR3和PYE在调节网络中起作用,该网络通过调节缺铁下的GLS积累来控制植物根部的病原体反应。
UNASSIGNED: ILR3 and
PYE function in a regulatory network that modulates GLS accumulation under iron deficiency. The molecular processes involved in the cross talk between iron (Fe) homeostasis and other metabolic processes in plants are poorly understood. In Arabidopsis thaliana the transcription factor IAA-LEUCINE RESISTANT3 (ILR3) regulates iron deficiency response, aliphatic glucosinolate (GLS) biosynthesis and pathogen response. ILR3 is also known to interact with its homolog, POPEYE (
PYE), which also plays a role in Fe response. However, little is known about how ILR3 regulates such diverse processes, particularly, via its interaction with
PYE. Since GLS are produced as part of a defense mechanism against wounding pathogens, we examined pILR3::β-GLUCURONIDASE expression and found that Fe deficiency enhances the wound-induced expression of ILR3 in roots and that ILR3 is induced in response to the wounding pathogen, sugarbeet root cyst nematode (Heterodera schachtii). We also examined the expression pattern of genes involved in Fe homeostasis and aliphatic GLS biosynthesis in pye-1, ilr3-2 and
pye-1xilr3-2 (pxi) mutants and found that ILR3 and
PYE differentially regulate the expression of genes involved these processes under Fe deficiency. We measured GLS levels and sugarbeet root cyst nematode infection rates under varying Fe conditions, and found that long-chain GLS levels are elevated in ilr3-2 and pxi mutants. This increase in long-chain GLS accumulation is correlated with elevated nematode resistance in ilr3-2 and pxi mutants in the absence of Fe. Our findings suggest that ILR3 and
PYE function in a regulatory network that controls wounding pathogen response in plant roots by modulating GLS accumulation under iron deficiency.