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ARS Home » Northeast Area » Beltsville, Maryland (BARC) » Beltsville Agricultural Research Center » Animal Biosciences & Biotechnology Laboratory » Research » Publications at this Location » Publication #327822

Title: Analysis of differentially expressed genes in Necrotic Enteritis-infected Fayoumi chicken using RNA-Seq: next generation sequencing mRNA in Fayoumi chickens

item TRUONG, AHN DUC - Chung-Ang University
item HONG, YEOJIN - Chung-Ang University
item PARK, BOYEONG - Chung-Ang University
item HOANG, CONG THANH - Chung-Ang University
item Lillehoj, Hyun
item HONG, YEONG HO - Chung-Ang University

Submitted to: Poultry Science
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 10/24/2016
Publication Date: 4/25/2017
Publication URL:
Citation: Truong, A., Hong, Y., Park, B., Hoang, C., Lillehoj, H.S., Hong, Y. 2017. Analysis of differentially expressed genes in Necrotic Enteritis-infected Fayoumi chicken using RNA-Seq: next generation sequencing mRNA in Fayoumi chickens. Poultry Science. 54(2):121-133.

Interpretive Summary: Necrotic enteritis (NE) is an enteric disease caused by Clostridium perfringens and represents a global problem that costs over USD 2 billion per year in production losses. High-throughput RNA sequencing (RNA-Seq) which is a powerful tool was used in this study to identify genes that control poultry response to this infection. Genomic analysis of the expressed genes located different functional categories of poultry genes in the intestinal mucosa of the NE-afflicted chickens. These new data identified many host genes associated with immune response and host defense against pathogens and strongly suggest important role of cell-mediated immunity in protective host response to NE. Application of high technology in genomic analysis will continue to impact our understanding the mechanisms of disease resistance to NE, and will foster the development of effective control strategies against these enteric pathogens.

Technical Abstract: We identified and evaluated differentially expressed genes (DEGs) by RNA-Seq in the intestinal mucosa of two Fayoumi chicken lines, M5.1 and M15.2, that are affected by necrotic enteritis (NE); these chicken lines share the same genetic background but have different major histocompatibility complexes (MHC). RNA-Seq generated over 49 and 40 million reads for lines M5.1 and M15.2, respectively. The alignment of these sequences with the Gallus gallus genome database revealed the expression of more than 14,500 gene transcripts in the two lines, among which 581 DEGs (308 were upregulated and 273 were downregulated), 1270 DEGs (1078 were upregulated and 192 were downregulated), and 1140 DEGs (1065 were upregulated and 75 were downregulated) were detected when lines M15.2 and M5.1 were compared with the control and compared between each other. The analysis of all DEGs using the gene ontology database revealed annotations for 111 biological processes, 32 cellular components, and 17 molecular functions, and KEGG pathway mapping indicated that the DEGs were primarily involved in immunity, responses to various stimuli, and signal transduction. In addition, we analyzed 183 innate immune genes that were differentially expressed in the NE-induced chicken lines, including 46 CD molecular genes, 89 immune-related genes, and 13 ß-defensin genes with three lineage-specific duplications. Taken together, the transcriptional profiles showed that line M5.1 was more resistant to NE than line M15.2 and that differential gene expression patterns were associated with host genetic differences in resistance to NE. qRT-PCR and RNA-Seq analyses showed that all the genes examined had similar responses to NE (correlation coefficient R = 0.84 to 0.88, p < 0.01) in both lines M5.1 and M15.2. To the best of our knowledge, this is the first study that describes NE-induced DEGs using RNA-seq in two Fayoumi chicken lines with different levels of susceptibility to NE. These results will lead to increased insights on NE disease resistance mechanisms and the role of host genes in the control of the host immune response.