The Understanding of the Plant Iron Deficiency Responses in Strategy I Plants and the Role of Ethylene in This Process by Omic Approaches

Abstract

Iron (Fe) is an essential plant micronutrient but is toxic in excess. Fe deficiency chlorosis is a major constraint for plant growth and causes severe losses of crop yields and quality. Under Fe deficiency conditions, plants have developed sophisticated mechanisms to keep cellular Fe homeostasis via various physiological, morphological, metabolic, and gene expression changes to facilitate the availability of Fe. Ethylene has been found to be involved in the Fe deficiency responses of plants through pharmacological studies or by the use of ethylene mutants. However, how ethylene is involved in the regulations of Fe starvation responses remains not fully understood. Over the past decade, omics approaches, mainly focusing on the RNA and protein levels, have been used extensively to investigate global gene expression changes under Fe-limiting conditions, and thousands of genes have been found to be regulated by Fe status. Similarly, proteome profiles have uncovered several hallmark processes that help plants adapt to Fe shortage. To find out how ethylene participates in the Fe deficiency response and explore putatively novel regulators for further investigation, this review emphasizes the integration of those genes and proteins, derived from omics approaches, regulated both by Fe deficiency, and ethylene into a systemic network by gene co-expression analysis.

Keywords: co-expression; ethylene; iron deficiency; proteomics; transcriptomics.

Figure 1

Venn diagram of the overlap of the iron deficiency response genes among the data sets for defining the conserved iron starvation response genes. (A) upregulated genes; (B) downregulated genes; (C,D) Gene ontology enrichment analysis (biological process, P < 0.001) of the overlap genes, 61 and 10, from the up- and down-regulated genes under iron starvation among the four data sets, respectively.

Figure 2

Coexpression network of the conserved iron deficiency induced genes. (A) Pair-wise coexpression relationships were calculated with the MACCU toolbox as described by Lin et al. (2011) using a Pearson coefficient cut-off of P ≧ 0.7. Nodes in diamond filled in green color indicate ethylene regulated genes; (B) Gene ontology (GO) enrichment analysis (biological process, P < 0.01) of the genes from the network in (A).

Figure 3

Methionine (Met) salvage cycle and ethylene, nicotianamine (NA), phtosiderophore (PS), and polyamine (PA) synthesis associated with proteins that are differentially accumulated upon Fe deficiency. As a central metabolite, SAM (S-adenosyl-methionine) is synthesized by SAMS (S-adenosylmethionine synthetase) from Met. Followed, SAM can be converted to MTA (methylthioadenosine) and ACC (aminocyclopropane-1-carboxylate) that is further converted to ethylene. SAM is also a precursor of PA and NA, which is converted to PS in Strategy II plant species. KMTB, 2-keto-4-methylthiobutyrate; MTR-P, methylthioribose phosphate; ARD, acireductone dioxygenase; ACS, ACC synthase; MTK, 5-methylthioribose kinase; DEP1, EHYDRATASE-ENOLASE-PHOSPHATASE-COMPLEX1; ACO, ACC oxidase.