Abstract
BackgroundGenetic resistance in cattle is considered a suitable way to control tick burden and its consequent losses for livestock production. Exploring tick-resistant (R) and tick-susceptible (S) hosts, we investigated the genetic mechanisms underlying the variation of Braford resistance to tick infestation. Skin biopsies from four-times-artificially infested R (n = 20) and S (n = 19) hosts, obtained before the first and 24 h after the fourth tick infestation were submitted to RNA-Sequencing. Differential gene expression, functional enrichment, and network analysis were performed to identify genetic pathways and transcription factors (TFs) affecting host resistance.ResultsIntergroup comparisons of hosts before (Rpre vs. Spre) and after (Rpost vs. Spost) tick infestation found 51 differentially expressed genes (DEGs), of which almost all presented high variation (TopDEGs), and 38 were redundant genes. Gene expression was consistently different between R and S hosts, suggesting the existence of specific anti-tick mechanisms. In the intragroup comparisons, Rpost vs. Rpre and Spost vs. Spre, we found more than two thousand DEGs in response to tick infestation in both resistance groups. Redundant and non-redundant TopDEGs with potential anti-tick functions suggested a role in the development of different levels of resistance within the same breed. Leukocyte chemotaxis was over-represented in both hosts, whereas skin degradation and remodeling were only found in TopDEGs from R hosts. Also, these genes indicated the participation of cytokines, such as IL6 and IL22, and the activation of Wingless (WNT)-signaling pathway. A central gene of this pathway, WNT7A, was consistently modulated when hosts were compared. Moreover, the findings based on a genome-wide association study (GWAS) corroborate the prediction of the WNT-signaling pathway as a candidate mechanism of resistance. The regulation of immune response was the most relevant pathway predicted for S hosts. Members of Ap1 and NF-kB families were the most relevant TFs predicted for R and S, respectively.ConclusionThis work provides indications of genetic mechanisms presented by Braford cattle with different levels of resistance in response to tick infestation, contributing to the search of candidate genes for tick resistance in bovine.
Highlights
Genetic resistance in cattle is considered a suitable way to control tick burden and its consequent losses for livestock production
No differences among groups were observed for the mapping statistics with the reads presenting around 70% concomitant pair alignment rate at the gene level
Regarding S hosts, we found the over-expression of the cytokine receptor activator of nuclear factor kappa-B ligand (RANKL) transcript and the absence of mRNAs corresponding to critical cytokines coding genes in skin inflammation, such as interleukin 6 (IL6) and interleukin 22 (IL22)
Summary
Genetic resistance in cattle is considered a suitable way to control tick burden and its consequent losses for livestock production. Cattle are the preferential hosts of Rhipicephalus microplus, a hard tick that attaches to the host skin and feeds for three weeks. Tick attachment and feeding depend upon numerous saliva components that inhibit host hemostatic responses to the parasite bites [1], a process that is the result of millions of years of evolution [2]. Rhipicephalus microplus is the most important ectoparasite of livestock, especially in tropical and subtropical areas [3], causing severe illness in cattle [4], with annual global costs of around US$ 22–30 billion [5]. Acaricides are currently the most common tick control method. Vaccination is an alternative for tick control, and several efforts have been conducted to
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