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J Plant Physiol. 2017 Oct;217:49-56. doi: 10.1016/j.jplph.2017.06.014. Epub 2017 Jul 4.

Transcriptional response of the extremophile red alga Cyanidioschyzon merolae to changes in CO2 concentrations.

Author information

1
Institute of Plant Biochemistry, Cluster of Excellence on Plant Sciences (CEPLAS), Heinrich Heine University, Universitätsstraße 1, 40225 Düsseldorf, Germany.
2
Leibniz-Institut für Pflanzengenetik und Kulturpflanzenforschung (IPK), Corrensstraße 3, 06466 Stadt Seeland, OT Gatersleben, Germany.
3
Institute of Plant Biochemistry, Cluster of Excellence on Plant Sciences (CEPLAS), Heinrich Heine University, Universitätsstraße 1, 40225 Düsseldorf, Germany. Electronic address: m.eisenhut@hhu.de.

Abstract

Cyanidioschyzon merolae (C. merolae) is an acidophilic red alga growing in a naturally low carbon dioxide (CO2) environment. Although it uses a ribulose 1,5-bisphosphate carboxylase/oxygenase with high affinity for CO2, the survival of C. merolae relies on functional photorespiratory metabolism. In this study, we quantified the transcriptomic response of C. merolae to changes in CO2 conditions. We found distinct changes upon shifts between CO2 conditions, such as a concerted up-regulation of photorespiratory genes and responses to carbon starvation. We used the transcriptome data set to explore a hypothetical CO2 concentrating mechanism in C. merolae, based on the assumption that photorespiratory genes and possible candidate genes involved in a CO2 concentrating mechanism are co-expressed. A putative bicarbonate transport protein and two α-carbonic anhydrases were identified, which showed enhanced transcript levels under reduced CO2 conditions. Genes encoding enzymes of a PEPCK-type C4 pathway were co-regulated with the photorespiratory gene cluster. We propose a model of a hypothetical low CO2 compensation mechanism in C. merolae integrating these low CO2-inducible components.

KEYWORDS:

CO(2) limitation; Cyanidioschyzon merolae; Photorespiration; RNA-seq

PMID:
28705662
DOI:
10.1016/j.jplph.2017.06.014
[Indexed for MEDLINE]

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