Transcriptome changes of blue-green algae, Arthrospira sp. in response to sulfate stress

Abstract

Arthrospira platensis, a protein-rich blue-green alga is utilized as feed supplements for human and animals, which primarily depend upon nutrients such as carbon, nitrogen, phosphorus and sulfur in the presence of sunlight for their growth and survival. Cyanobacteria depend on sulfur for the synthesis and modification of a variety of biomolecules but, the exact mechanism of sulfur metabolism and impact of sulfate deprivation on A. platensis remain unclear. In this study, we analysed the change in growth and difference in the expression of key molecules of A. platensis during sulfate deprivation by comparing the transcriptome profiles of A. platensis grown at normal and sulfur deprived culture conditions. Observations showed that sulfate stress affected the levels of pigments in spirulina with slightly reduced growth. Transcriptome profile showed that expression profiles of different genes involved in various sulfur-dependent pathways were altered due to sulfur depletion. Major genes that were down-regulated include iron-sulfur clusters biosynthesis due to the absence of sulfur. Expression of genes involved in pathways such as translation, amino acid biosynthesis, protein folding, rRNA binding, were down-regulated, whereas genes involved in carbohydrate metabolism, phosphor relay sensor kinase activity, integral components of membrane, plasma membrane, thylakoid membrane, metal ion binding and DNA repair, were up-regulated during sulfur stress. Genes involved in transcription were up-regulated and hence there is a higher number of transcripts in A. platensis grown in sulfur depleted state. However, genes involved in translation were down-regulated; thus, there was a reduction in total protein content. Based on this analysis, it could be concluded that A. platensis was able to sustain sulfate stress, by its ability to alter the expression of genes that are specifically involved in sulfur metabolism and various other sulfur-dependent pathways.