Figure 4.

Basic cellular changes at low-iron. Differential gene expression of exponentially growing iron-limited versus iron-replete T. oceanica cells was assessed from global transcriptomics and proteomics approaches. (a) Transcriptomics data were screened with T-ACE, a transcriptome database browser that plots the assembled transcript fragments according to their differential regulation as inferred from differential read contribution of Fe(-) and Fe(+) libraries to each transcript contig. (b) For the proteomics data the differential regulation of each gene product is represented by the median of all PBC (peptide/SDS-PAGE band/charge) ratios assigned to it, with error bars constructed from the first and third quartiles. The main plot shows proteins with at least two PBC values, inset contains proteins with a single PBC value. (c) Only a subset of low-iron responsive genes could be assigned a robust annotation and were suitable for mapping to a cellular scheme. Accordingly, the cellular response of T. oceanica to low-iron was inferred from the mapping of a representative selection of genes (see text) and their respective differential regulation on the transcript and protein levels. The most pronounced elements of the complex response are chloroplast retrenchment (chlorosis) and the consequential take-over of energy metabolism by the mitochondrial system (metabolic shift). Diverse surface-related binding capacities and the potential for degrading organic matter are enhanced, suggesting a putative mixotrophic response (mixotrophy). The strongest transcriptional response is seen from genes involved in iron-uptake or compensational substitutions (4). This iron-specific part of the cellular response may be mediated by a conserved promoter motif identified in this work. CC, Calvin-Benson-Bassham cycle; CP, chloroplast; MT, mitochondria; TCA, tricarboxylic acid cycle; TF, transcription factor.