Transcriptome profiling and digital gene expression analysis of sweet potato for the identification of putative genes involved in the defense response against Fusarium oxysporum f. sp. batatas.

Yuli Lin,Yuli Lin,Yuli Lin,Weikun Zou,Songliang Wang,Xuanyang Chen,Xuanyang Chen,Xuanyang Chen,Shiqiang Lin,Haizhou Chen,Zhijian Yang,Dennis Onofua,Shiqiang Lin,T R Ganapathi

doi:10.1371/journal.pone.0187838

Abstract

Sweet potato production is constrained by Fusarium wilt, which is caused by Fusarium oxysporum f. sp. batatas (Fob). The identification of genes related to disease resistance and the underlying mechanisms will contribute to improving disease resistance via sweet potato breeding programs. In the present study, we performed de novo transcriptome assembly and digital gene expression (DGE) profiling of sweet potato challenged with Fob using Illumina HiSeq technology. In total, 89,944,188 clean reads were generated from 12 samples and assembled into 101,988 unigenes with an average length of 666 bp; of these unigenes, 62,605 (61.38%) were functionally annotated in the NCBI non-redundant protein database by BLASTX with a cutoff E-value of 10−5. Clusters of Orthologous Groups (COG), Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) annotations were examined to explore the unigenes’ functions. We constructed four DGE libraries for the sweet potato cultivars JinShan57 (JS57, highly resistant) and XinZhongHua (XZH, highly susceptible), which were challenged with pathogenic Fob. Genes that were differentially expressed in the four libraries were identified by comparing the transcriptomes. Various genes that were differentially expressed during defense, including chitin elicitor receptor kinase 1 (CERK), mitogen-activated protein kinase (MAPK), WRKY, NAC, MYB, and ethylene-responsive transcription factor (ERF), as well as resistance genes, pathogenesis-related genes, and genes involved in salicylic acid (SA) and jasmonic acid (JA) signaling pathways, were identified. These data represent a sequence resource for genetic and genomic studies of sweet potato that will enhance the understanding of the mechanism of disease resistance.

Highlights

Sweet potato is the 7th most important crop globally, with an annual area harvest of 8.0 million ha and a total global production of 104.5 million tons
The production of sweet potato is constrained by Fusarium wilt, which is caused by Fusarium oxysporum f. sp. batatas (Fob) [4]
To comprehensively generate the transcriptome and obtain insights into the molecular mechanisms involved in the resistance of sweet potato to Fusarium wilt, the total RNA from the stems of the highly resistant cultivar JinShan 57 (JS57) and highly susceptible cultivar XZH was isolated

Summary

Introduction

Sweet potato is the 7th most important crop globally, with an annual area harvest of 8.0 million ha and a total global production of 104.5 million tons. Sweet potato is planted primarily in developing areas in Asia and Africa [1, 2]. In the USA, the harvest area has increased from 33.3 kha in 2002 to 54.7 kha in 2014, and this increase has resulted in a corresponding increase in sweet potato production from 580.5 kilotons to 1.34 million tons [2]. A soil-borne pathogenic fungus, is classified into more than 120 formae speciales and races, each of which infects one specific crop, such as sweet potato, tomato, banana, watermelon or pepper. The production of sweet potato is constrained by Fusarium wilt, which is caused by Fusarium oxysporum f. Fusarium wilt has spread across many provinces in Central China and threatens sweet potato production [7]

Methods

Results

Discussion

Conclusion