Mohandas Snigdha1, Duraisamy Prasath2. 1. ICAR-Indian Institute of Spices Research, Kozhikode, Kerala, 673012, India. 2. ICAR-Indian Institute of Spices Research, Kozhikode, Kerala, 673012, India. prasath.d@icar.gov.in.
Abstract
BACKGROUND: Bacterial wilt is the most devastating disease in ginger caused by Ralstonia solanacearum. Even though ginger (Zingiber officinale) and mango ginger (Curcuma amada) are from the same family Zingiberaceae, the latter is resistant to R. solanacearum infection. MicroRNAs have been identified in many crops which regulates plant-pathogen interaction, either through silencing genes or by blocking mRNA translation. However, miRNA's vital role and its targets in mango ginger in protecting bacterial wilt is not yet studied extensively. In the present study, using the "psRNATarget" server, we analyzed available ginger (susceptible) and mango ginger (resistant) transcriptome to delineate and compare the microRNAs (miRNA) and their target genes (miRTGs). RESULTS: A total of 4736 and 4485 differential expressed miRTGs (DEmiRTGs) were identified in ginger and mango ginger, respectively, in response to R. solanacearum. Functional annotation results showed that mango ginger had higher enrichment than ginger in top enriched GO terms. Among the DEmiRTGs, 2105 were common in ginger and mango ginger. However, 2337 miRTGs were expressed only in mango ginger which includes 62 defence related and upregulated miRTGs. We also identified 213 miRTGs upregulated in mango ginger but downregulated in ginger, out of which 23 DEmiRTGS were defence response related. We selected nine miRNA/miRTGs pairs from the data set of common miRTGs of ginger and mango ginger and validated using qPCR. CONCLUSIONS: Our data covered the expression information of 9221 miRTGs. We identified nine miRNA/miRTGs key candidate pairs in response to R. solanacearum infection in ginger. This is the first report of the integrated analysis of miRTGs and miRNAs in response to R. solanacearum infection among ginger species. This study is expected to deliver several insights in understanding the miRNA regulatory network in ginger and mango ginger response to bacterial wilt.
BACKGROUND: Bacterial wilt is the most devastating disease in ginger caused by Ralstonia solanacearum. Even though ginger (Zingiber officinale) and mangoginger (Curcuma amada) are from the same family Zingiberaceae, the latter is resistant to R. solanacearuminfection. MicroRNAs have been identified in many crops which regulates plant-pathogen interaction, either through silencing genes or by blocking mRNA translation. However, miRNA's vital role and its targets in mangoginger in protecting bacterial wilt is not yet studied extensively. In the present study, using the "psRNATarget" server, we analyzed available ginger (susceptible) and mangoginger (resistant) transcriptome to delineate and compare the microRNAs (miRNA) and their target genes (miRTGs). RESULTS: A total of 4736 and 4485 differential expressed miRTGs (DEmiRTGs) were identified in ginger and mangoginger, respectively, in response to R. solanacearum. Functional annotation results showed that mangoginger had higher enrichment than ginger in top enriched GO terms. Among the DEmiRTGs, 2105 were common in ginger and mangoginger. However, 2337 miRTGs were expressed only in mangoginger which includes 62 defence related and upregulated miRTGs. We also identified 213 miRTGs upregulated in mangoginger but downregulated in ginger, out of which 23 DEmiRTGS were defence response related. We selected nine miRNA/miRTGs pairs from the data set of common miRTGs of ginger and mangoginger and validated using qPCR. CONCLUSIONS: Our data covered the expression information of 9221 miRTGs. We identified nine miRNA/miRTGs key candidate pairs in response to R. solanacearuminfection in ginger. This is the first report of the integrated analysis of miRTGs and miRNAs in response to R. solanacearuminfection among ginger species. This study is expected to deliver several insights in understanding the miRNA regulatory network in ginger and mangoginger response to bacterial wilt.