Lin Xian Yong, Ye Yi Quan, Fan Shi Kai, Jin Chong Wei, Zheng Shao Jian
Key Laboratory of Environment Remediation and Ecological Health, College of Natural Resource and Environmental Sciences, Zhejiang University, Hangzhou 310058, China (X.Y.L., Y.Q.Y., S.K.F., C.W.J.); andState Key Laboratory of Plant Physiology and Biochemistry, College of Life Sciences, Zhejiang University, Hangzhou 310058, PR China (S.J.Z.).
Key Laboratory of Environment Remediation and Ecological Health, College of Natural Resource and Environmental Sciences, Zhejiang University, Hangzhou 310058, China (X.Y.L., Y.Q.Y., S.K.F., C.W.J.); andState Key Laboratory of Plant Physiology and Biochemistry, College of Life Sciences, Zhejiang University, Hangzhou 310058, PR China (S.J.Z.)
Plant Physiol. 2016 Feb;170(2):907-20. doi: 10.1104/pp.15.01598. Epub 2015 Dec 7.
Previous studies have identified that auxins acts upstream of nitric oxide in regulating iron deficiency responses in roots, but the upstream signaling molecule of auxins remains unknown. In this study, we showed that Fe deficiency increased sucrose (Suc) level in roots of Arabidopsis (Arabidopsis thaliana). Exogenous application of Suc further stimulated Fe deficiency-induced ferric-chelate-reductase (FCR) activity and expression of Fe acquisition-related genes FRO2, IRT1, and FIT in roots. The opposite patterns were observed in the dark treatment. In addition, FCR activity and expression of Fe acquisition-related genes were higher in the Suc high-accumulating transgenic plant 35S::SUC2 but were lower in the Suc low-accumulating mutant suc2-5 compared with wild-type plants under Fe-deficient conditions. Consequently, Fe deficiency tolerance was enhanced in 35S::SUC2 but was compromised in suc2-5. Exogenous Suc also increased root β-glucuronidase (GUS) activity in auxin-inducible reporter DR5-GUS transgenic plants under Fe deficiency. However, exogenous Suc failed to increase FCR activity and expression of Fe acquisition-related genes in the auxin transport-impaired mutants aux1-7 and pin1-1 as well as in the wild-type plants treated with an auxin transport inhibitor under Fe deficiency. In summary, we found that increased Suc accumulation is required for regulating Fe deficiency responses in plants, with auxins acting downstream in transmitting the Fe deficiency signal.
先前的研究已确定,在调节根系缺铁反应中,生长素作用于一氧化氮的上游,但生长素的上游信号分子仍不清楚。在本研究中,我们发现缺铁会增加拟南芥根系中的蔗糖(Suc)水平。外源施加蔗糖进一步刺激了缺铁诱导的根系中铁螯合物还原酶(FCR)活性以及铁吸收相关基因FRO2、IRT1和FIT的表达。在黑暗处理中观察到相反的模式。此外,在缺铁条件下,与野生型植株相比,蔗糖高积累转基因植株35S::SUC2中的FCR活性和铁吸收相关基因的表达较高,而蔗糖低积累突变体suc2-5中的FCR活性和铁吸收相关基因的表达较低。因此,35S::SUC2的缺铁耐受性增强,而suc2-5的缺铁耐受性受损。在缺铁条件下,外源蔗糖还增加了生长素诱导型报告基因DR5-GUS转基因植株根系中的β-葡萄糖醛酸酶(GUS)活性。然而,外源蔗糖未能增加缺铁条件下生长素运输受损突变体aux1-7和pin1-1以及用生长素运输抑制剂处理的野生型植株中的FCR活性和铁吸收相关基因的表达。总之,我们发现蔗糖积累增加是调节植物缺铁反应所必需的,生长素在传递缺铁信号中作用于下游。