The mechanism of Populus tomentosa in response to iron deficiency

Iron (Fe) is an essential micronutrient for the survival and proliferation of plants. Plants have evolved complex mechanisms to maintain Fe homeostasis in response of Fe deficiency conditions. To explore the mechanisms of Populus tomentosa response to Fe deficiency, we evaluated the physiological, biochemical and transcriptome differences of P. tomentosa between Fe-sufficient and Fe-deficient conditions. The results showed that, under Fe-free conditions, the chlorophyll synthesis and photosynthesis pathways in shoots were extremely depressed. The inhibition of these pathways caused chlorosis and supression of photosynthesis, which hindered the shoot growth eventually. Although both two photosynthetic systems (PSI and PSII) were inhibited under Fe limited conditons, PSI is affected more serious and earlier than PSII. In order to maintain Fe homeostasis, several genes involved in Fe regulation network were differentially expressed. At the late period of Fe deficiency response, in roots, a part of genes (BTS, bHLH38/39 and PYE) in PYE regulatory network were all up-regulated, while some genes (EIN3, ERF and FIT) belonging to root-specific ethylene-dependent FIT regulatory network were all down-regulated. It indicated that at the Fe-deficiency late stage, in P. tomentosa roots, only the PYE regulatory network was active for Fe homeostasis regulation, whereas the FIT network was inhibited. Moreover, FRO2 was induced in P. tomentosa roots to reduce more Fe3+, which is similar with other strategy I plants. But at the Fe-deficiency late stage, for the Fe2+ uptake process, the major Fe2+ transporter gene (IRT1) was not differentially expressed, only another Fe2+ transporter gene(NRAMP1) was induced to promote Fe2+ absorption.