Dataset Information

Meta-analyses of genome wide association studies in lines of laying hens divergently selected for feather pecking using imputed sequence level genotypes.

ABSTRACT:

Background

Feather pecking (FP) is damaging behavior in laying hens leading to global economic losses in the layer industry and massive impairments of animal welfare. The objective of the study was to discover genetic variants and affected genes that lead to FP behavior. To achieve that we imputed low-density genotypes from two different populations of layers divergently selected for FP to sequence level by performing whole genome sequencing on founder and half-sib individuals. In order to decipher the genetic structure of FP, genome wide association studies and meta-analyses of two resource populations were carried out by focusing on the traits 'feather pecks delivered' (FPD) and the 'posterior probability of a hen to belong to the extreme feather pecking subgroup' (pEFP).

Results

In this meta-analysis, we discovered numerous genes that are affected by polymorphisms significantly associated with the trait FPD. Among them SPATS2L, ZEB2, KCHN8, and MRPL13 which have been previously connected to psychiatric disorders with the latter two being responsive to nicotine treatment. Gene set enrichment analysis revealed that phosphatidylinositol signaling is affected by genes identified in the GWAS and that the Golgi apparatus as well as brain structure may be involved in the development of a FP phenotype. Further, we were able to validate a previously discovered QTL for the trait pEFP on GGA1, which contains variants affecting NIPA1, KIAA1211L, AFF3, and TSGA10.

Conclusions

We provide evidence for the involvement of numerous genes in the propensity to exhibit FP behavior that could aid in the selection against this unwanted trait. Furthermore, we identified variants that are involved in phosphatidylinositol signaling, Golgi metabolism and cell structure and therefore propose changes in brain structure to be an influential factor in FP, as already described in human neuropsychiatric disorders.

SUBMITTER: Falker-Gieske C

PROVIDER: S-EPMC7528462 | biostudies-literature | 2020 Oct

REPOSITORIES: biostudies-literature

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Meta-analyses of genome wide association studies in lines of laying hens divergently selected for feather pecking using imputed sequence level genotypes.

Falker-Gieske Clemens C Iffland Hanna H Preuß Siegfried S Bessei Werner W Drögemüller Cord C Bennewitz Jörn J Tetens Jens J

BMC genetics 20201001 1

<h4>Background</h4>Feather pecking (FP) is damaging behavior in laying hens leading to global economic losses in the layer industry and massive impairments of animal welfare. The objective of the study was to discover genetic variants and affected genes that lead to FP behavior. To achieve that we imputed low-density genotypes from two different populations of layers divergently selected for FP to sequence level by performing whole genome sequencing on founder and half-sib individuals. In order ...[more]

PMID: 33004014

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Project description:Feather pecking in chickens is a damaging behavior, seriously impacting animal welfare and leading to economic losses. Feather pecking is a complex trait, which is partly under genetic control. Different hypotheses have been proposed to explain the etiology of feather pecking and notably, several studies have identified similarities between feather pecking and human mental disorders such as obsessive-compulsive disorder and schizophrenia. This study uses transcriptomic and phenotypic data from 167 chickens to map expression quantitative trait loci and to identify regulatory genes with a significant effect on this behavioral disorder using an association weight matrix approach. From 70 of the analyzed differentially expressed genes, 11,790 genome wide significantly associated variants were detected, of which 23 showed multiple associations (≥15). These were located in proximity to a number of genes, which are transcription regulators involved in chromatin binding, nucleic acid metabolism, protein translation and putative regulatory RNAs. The association weight matrix identified 36 genes and the two transcription factors: SP6 (synonym: KLF14) and ENSGALG00000042129 (synonym: CHTOP) as the most significant, with an enrichment of KLF14 binding sites being detectable in 40 differentially expressed genes. This indicates that differential expression between animals showing high and low levels of feather pecking was significantly associated with a genetic variant in proximity to KLF14. This multiallelic variant was located 652 bp downstream of KLF14 and is a deletion of 1-3 bp. We propose that a deletion downstream of the transcription factor KLF14 has a negative impact on the level of T cells in the developing brain of high feather pecking chickens, which leads to developmental and behavioral abnormalities. The lack of CD4 T cells and gamma-Aminobutyric acid (GABA) receptors are important factors for the increased propensity of laying hens to perform feather pecking. As such, KLF14 is a clear candidate regulator for the expression of genes involved in the pathogenic development. By further elucidating the regulatory pathways involved in feather pecking we hope to take significant steps forward in explaining and understanding other mental disorders, not just in chickens.

Project description:BackgroundFeather pecking (FP) is a maladaptive behavior in laying hens that is associated with numerous physiological traits, including those involving the central neurotransmitter system and the immune system, which have been identified in many species as being regulated by the gut microbiota via the "microbiota-gut-brain" (MGB) axis. Yet, it is unknown whether and how gut microbiota influences FP by regulating multiple central neurotransmission systems and immune system.MethodsThis study was measured the prevalence of severe FP (SFP) in the commercial layer farm. The chicken flock with the highest frequency of SFP were selected for FP phenotype identification. Nontargeted metabolomics was performed to investigated the differences in the peripheral and central metabolites and 16S rDNA sequencing was performed to investigated the differences in gut microbiome of laying hens with different FP phenotypes. Correlation analysis was performed to determine the potential mechanism by which the disturbed gut microbiota may modulate host physiology and behavior.ResultsThe results showed that pullets (12 weeks of age) showed significantly higher SFP frequencies than chicks (6 weeks of age) and adults (22 weeks of age; p < 0.05). Compared to neutrals (N), peckers (P) exhibited the stress-induced immunosuppression with the increased plasma levels of corticosterone and norepinephrine, and the decreased plasma levels of IgA, IL-1, IL-6 and tumor necrosis factor α (p < 0.05). In the cecum, the relative abundances of Bacteroides and Gemmiger were higher in the P group, while Roseburia, Ruminococcus2, Anaerostipes, Lachnospiracea_incertae_sedis and Methanobrevibacter were more enriched in the N group. Moreover, increased plasma levels of L-tryptophan, beta-tyrosine and L-histidine were found in the P group (p < 0.05). Notably, in the P group, hippocampal levels of L-tryptophan, xanthurenic acid, L-histidine and histamine were improved and showed a positive association with L-glutamic acid levels. Plasma levels of L-tryptophan, beta-tyrosine and L-histidine were both positively correlated with Bacteroides abundance but negatively correlated with Methanobrevibacter abundance.ConclusionOverall, these findings suggest that the development of FP may be affected by the gut microbiota, which regulates the central glutamatergic nerve system by altering the metabolism of tryptophan, histidine and tyrosine.

Dataset Information

Meta-analyses of genome wide association studies in lines of laying hens divergently selected for feather pecking using imputed sequence level genotypes.

Background

Results

Conclusions

Publications

Meta-analyses of genome wide association studies in lines of laying hens divergently selected for feather pecking using imputed sequence level genotypes.

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