Abstract
BackgroundIron (Fe) and phosphorus (P) are essential mineral nutrients in plants. Knowledge regarding global changes in the abundance of Fe-responsive genes under Pi deficiency as well as the processes these genes are involved in remains largely unavailable at the genome level. In the current study, we comparatively analyzed RNA sequencing data sets relative to Fe deficiency (NCBI: SRP044814) and Pi starvation (NCBI: SRA050356.1).ResultsAnalysis showed a total of 579 overlapping genes that are responsible for both Fe deficiency and Pi starvation in Arabidopsis roots. A subset of 137 genes had greater than twofold changes in transcript abundant as a result of the treatments. Gene ontology (GO) analysis showed that the stress-related processes ‘response to salt stress’, ‘response to oxidative stress’, and ‘response to zinc ion’ were enriched in the 579 genes, while Fe response-related processes, including ‘cellular response to nitric oxide’, ‘cellular response to iron ion’, and ‘cellular iron ion homeostasis’, were also enriched in the subset of 137 genes. Co-expression analysis of the 579 genes using the MACCU toolbox yielded a network consisting of 292 nodes (genes). Further analysis revealed that a subset of 90 genes were up-regulated under Fe shortage, but down-regulated under Pi starvation. GO analysis in this group of genes revealed an increased cellular response to iron ion/nitric oxide/ethylene stimuli. Promoter analysis was performed in 35 of the 90 genes with a 1.5-fold or greater change in abundance, showing that 12 genes contained the PHOSPHATE STARVATION RESPONSE1-binding GNATATNC cis-element within their promoter regions. Quantitative real-time PCR showed that the decreased abundance of Fe acquisition genes under Pi deficiency exclusively relied on Fe concentration in Pi-deficient media.ConclusionsComprehensive analysis of the overlapping genes derived from Fe deficiency and Pi starvation provides more information to understand the link between Pi and Fe homeostasis. Gene clustering and root-specific co-expression analysis revealed several potentially important genes which likely function as putative novel players in response to Fe and Pi deficiency or in cross-talk between Fe-deficient responses and Pi-deficient signaling.Electronic supplementary materialThe online version of this article (doi:10.1186/s13104-015-1524-y) contains supplementary material, which is available to authorized users.
Highlights
IntroductionKnowledge regarding global changes in the abundance of Fe-responsive genes under Pi deficiency as well as the processes these genes are involved in remains largely unavailable at the genome level
Iron (Fe) and phosphorus (P) are essential mineral nutrients in plants
Down‐regulation of Fe‐acquisition genes upon Pi deficiency is dependent on Fe concentration in the media To determine how Fe acquisition genes are down-regulated by Pi deficiency and whether this down-regulation is dependent on PHOSPHATE STARVATION RESPONSE1 (PHR1), we investigated changes in genes that were most induced by Fe deficiency at the transcript level in wild type and the phr1 mutant under varied growth conditions as follows: Pi deficiency
Summary
Knowledge regarding global changes in the abundance of Fe-responsive genes under Pi deficiency as well as the processes these genes are involved in remains largely unavailable at the genome level. Under Fe-deficient conditions, Arabidopsis (Arabidopsis thaliana) and other dicotyledonous and non-graminaceous monocotyledonous plants use a reduction strategy, referred to as strategy I [10], to increase Fe bioavailability. In this strategy, acidification of the rhizosphere mediated by the H+-translocating P-type ATPase AHA2 [6, 11] occurs as the first step, which leads to an increase in the concentration of chelated Fe(III). Recent studies have shown that the transcription factors bHLH100 and bHLH101, which belong to the Ib sub-group of bHLH proteins, are involved in Arabidopsis Fe deficiency responses by interacting with FIT [20] or via a FIT-independent manner [21]
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