Author
Marancik, David | |
Gao, Guangtu | |
PANERU, BAM - Middle Tennessee State University | |
MA, HAO - West Virginia University | |
HERNANDEZ, ALVARO - University Of Illinois | |
SALEM, MOHAMED - Middle Tennessee State University | |
YAO, JIANBO - West Virginia University | |
Palti, Yniv | |
Wiens, Gregory - Greg |
Submitted to: Frontiers in Genetics
Publication Type: Peer Reviewed Journal Publication Acceptance Date: 12/11/2014 Publication Date: 1/8/2015 Citation: Marancik, D.P., Gao, G., Paneru, B., Ma, H., Hernandez, A.G., Salem, M., Yao, J., Palti, Y., Wiens, G.D. 2015. Whole-body transcriptome of selectively bred, resistant-, control-, and susceptible-line rainbow trout following experimental challenge with Flavobacterium psychrophilum. Frontiers in Genetics. 5(243):1-15. DOI:10.3389/fgene.2014.00453. Interpretive Summary: Selective breeding for disease resistance offers new opportunities for improving fish welfare in aquaculture. At our location, researchers have produced a line of rainbow trout with increased resistance against Flavobacterium psychrophilum, the cause of bacterial cold water disease (BCWD). The mechanisms governing this resistance are unknown. We compared gene expression in disease resistant, disease susceptible, and control fish after one day and five days post-infection with F. psychrophilum. Expression of 1884 genes were found to be either increased or decreased after infection. These included a large number of genes associated with the immune response. Compared to uninfected fish, there were more differentially expressed genes on day 5 post-infection than there were on day 1 which correlates with the presence of bacteria. Significant differences were found between resistant, control, and susceptible fish in both naive fish and fish infected with F. psychrophilum. These genes may be influenced by selective breeding and play a role in survival. This information is important because it characterizes the fish response to infection on a genetic level, demonstrates quantifiable differences between selectively bred fish, and suggests immune and physiologic mechanisms associated with survival. Technical Abstract: Genetic improvement for enhanced disease resistance in fish is an increasingly utilized approach to mitigate endemic infectious disease in aquaculture. In domesticated salmonid populations, large phenotypic variation in disease resistance has been identified but the genetic basis for altered responsiveness remains unclear. We previously reported three generations of selection and phenotypic validation of a bacterial cold water disease (BCWD) resistant line of rainbow trout, designated ARS-Fp-R. This line has higher survival after infection by either standardized laboratory challenge or natural challenge as compared to two reference lines, designated ARS-Fp-C (control) and ARS-Fp-S (susceptible). In this study, we utilized 1.1 g fry from the three genetic lines and performed RNA-seq to measure transcript abundance from the whole body of naive and Flavobacterium psychrophilum infected fish at day 1 (early time-point) and at day 5 post-challenge (onset of mortality). Sequences from 24 libraries were mapped onto the rainbow trout genome reference transcriptome of 46,585 predicted protein coding mRNAs that included 2633 putative immune-relevant gene transcripts. A total of 1884 genes (4.0% genome) exhibited differential transcript abundance between infected and mock-challenged fish (FDR < 0.05) that included chemokines, complement components, tnf receptor superfamily members, interleukins, nod-like receptor family members, and genes involved in metabolism and wound healing. The largest number of differentially expressed genes occurred on day 5 post-infection between naive and challenged ARS-Fp-S line fish correlating with high bacterial load. After excluding the effect of infection, we identified 21 differentially expressed genes between the three genetic lines. In summary, these data indicate global transcriptome differences between genetic lines of naive animals as well as differentially regulated transcriptional responses to infection. |