Transcriptome sequencing and whole genome expression profiling of purple-fleshed sweetpotato under salt stress

Abstract Abstract Background: Purple-fleshed sweetpotato (PFSP) is one of the most important crops in the word which helps to bridge the food gap and contribute to solve the malnutrition problem especially in developing countries. Salt stress is seriously limiting its production and distribution. Due to lacking of reference genome, transcriptome sequencing is offering a rapid approach for crop improvement with promising agronomic traits and stress adaptability. Results: Five cDNA libraries were prepared from the third true leaf of PFSP at seedlings stage (Xuzi-8 cultivar) treated with 200 mM NaCl for 0, 1, 6, 12, 48 hours. Using second and third generation technology, Illumina sequencing generated 170,344,392 clean high-quality long reads that were assembled into 15,998 unigenes with an average length 2178 base pair and 96.55% of these unigenes were functionally annotated in the NR protein database. A number of 537 unigenes failed to hit any homologs which may be considered as novel genes. The current results indicated that sweetpotato plants behavior during the first hour of salt stress was different than the other three time points. Furthermore, expression profiling analysis identified 4, 479, 281, 508 significantly expressed unigenes in salt stress treated samples at the different time points including 1, 6, 12, 48 hours, respectively as compared to control. COG analysis revealed that the highest number of genes was categorized as “post-translational modification, protein turnover, chaperones” followed by “signal transduction mechanisms”. Gene ontology (GO) enrichment analysis showed that salt stress caused changes in metabolic process (Secondary and amino acids), hormone response, cellular processes and single organism processes. These findings suggest that salt stress tolerance in PFSP plants may be mainly depended on three factors including the balance between protein biosynthesis and degradation, preventing or correcting damage caused by miss-folding due to salt stress and transforming the certain stimulus induced by salt stress into a biochemical signal which activates more genes specifically involved in salt stress tolerance.