Identification and functional characterization of genes influencing feather pecking in chickens
Feather pecking and cannibalism are frequent and serious problems in poultry, especially in laying hens. Feather loss and injuries massively impair animal welfare and lead to higher energy demands and thus lower resource efficiency. Up to now, feather pecking was mainly controlled by routine beak trimming, which itself is an animal welfare issue and is banned or will be banned in more and more countries including Germany. Feather pecking is a complex and multifactorial behavior trait and the exact causes are still largely unknown.
The aim of the project was the identification and functional characterization of genes influencing the propensity to perform feather pecking in laying hens. The work was conducted in divergently selected chicken lines, i.e. lines either exhibiting severe feather pecking or nearly no pecking at all. Based on previous results, these lines were used for the establishment of a resource population, which was deeply phenotyped and genotyped with dense marker panels. The genomes of founder animals were entirely sequenced and whole brain samples were used for transcriptome analyses by applying RNA sequencing.
We conducted multiple analyses involving whole genome sequencing, RNA sequencing, and Fluidigm analysis of two experimental populations – one F2 design and a half-sib population divergently selected for feather pecking over multiple generations. Genome-wide association studies and expression quantitative trait loci (eQTL) studies with SNPs, InDels, structural variants, and tandem repeats, as well as transcriptome studies directed at feather pecking behavior and the response to light lead to a comprehensive model for the behavior. Low GABA receptor density in the neurons of HFP chickens may be caused by a Dicer1 dysregulation, which leads to a shortage of miRNAs that regulate various GABA receptors. Furthermore, dysfunctional dystrophin could lead to impairment of GABA receptor clustering. Low GABA concentrations or responsiveness in the brains of HFP cause a constant high level of excitation and explain this obsessive compulsive-like behavior. Abnormal brain development in HFP may be caused by genetic variants in proximity to two transcription factors: KLF14 and ETV1. Genome-wide significant association of 40 differentially expressed genes, 10 of which involved in leukocyte biology, with a deletion downstream of KLF14 point towards a neurodevelopmental defect. Additionally, a tandem repeat located close to ETV1 implicates further involvement of T cells in the emergence of FP probably in conjunction with Smad4.
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