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#116908 - 11/09/17 04:00 PM Re: Journal papers online - reference list [Re: KazJaps]
Wieslaw Offline
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Registered: 09/18/09
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Sex Reversal and Comparative Data Undermine the W Chromosome and Support Z-linked DMRT1 as the Regulator of Gonadal Sex Differentiation in Birds.

https://www.ncbi.nlm.nih.gov/pubmed/28911174

Abstract

The exact genetic mechanism regulating avian gonadal sex differentiation has not been completely resolved. The most likely scenario involves a dosage mechanism, whereby the Z-linked DMRT1 gene triggers testis development. However, the possibility still exists that the female-specific W chromosome may harbor an ovarian determining factor. In this study, we provide evidence that the universal gene regulating gonadal sex differentiation in birds is Z-linked DMRT1 and not a W-linked (ovarian) factor. Three candidate W-linked ovarian determinants are HINTW, female-expressed transcript 1 (FET1), and female-associated factor (FAF). To test the association of these genes with ovarian differentiation in the chicken, we examined their expression following experimentally induced female-to-male sex reversal using the aromatase inhibitor fadrozole (FAD). Administration of FAD on day 3 of embryogenesis induced a significant loss of aromatase enzyme activity in female gonads and masculinization. However, expression levels of HINTW, FAF, and FET1 were unaltered after experimental masculinization. Furthermore, comparative analysis showed that FAF and FET1 expression could not be detected in zebra finch gonads. Additionally, an antibody raised against the predicted HINTW protein failed to detect it endogenously. These data do not support a universal role for these genes or for the W sex chromosome in ovarian development in birds. We found that DMRT1 (but not the recently identified Z-linked HEMGN gene) is male upregulated in embryonic zebra finch and emu gonads, as in the chicken. As chicken, zebra finch, and emu exemplify the major evolutionary clades of birds, we propose that Z-linked DMRT1, and not the W sex chromosome, regulates gonadal sex differentiation in birds.

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#116919 - 11/21/17 12:30 AM Re: Journal papers online - reference list [Re: KazJaps]
Redcap Offline
Ruler of the Roost

Registered: 08/14/06
Posts: 985
Loc: Germany
Kimball, E. (1953). Genetics of Buttercup Plumage Pattern in the Fowl, Poultry Science, Volume 32, Issue 4, 1 July 1953, Pages 683–692.
http://documents.kippenjungle.nl/#post50
Kimball, E. (1960). Differential Penciled Phenotypes & Genetic Origin of Penciled Pattern. Volume 39, Issue 1, 1 January 1960, Pages 232-234.
http://documents.kippenjungle.nl/#post49
_________________________

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#116953 - 12/10/17 05:40 PM Re: Journal papers online - reference list [Re: Redcap]
KazJaps Offline
Classroom Professor

Registered: 08/30/02
Posts: 2871
Loc: Australia
Posting again for easier reference to papers, abstracts & summaries...

To mutations that increase size - ie larger than Red Jungle Fowl.

Kerje et al. 2003.The twofold difference in adult size between the red junglefowl and White Leghorn chickens is largely explained by a limited number of QTLs. Anim Genet. 2003 Aug;34(4):264-74. -Abstract here
Quote:
The QTL analysis of growth traits revealed 13 loci that showed genome-wide significance. The four major growth QTLs explained 50 and 80% of the difference in adult body weight between the founder populations for females and males, respectively. A major QTL for growth, located on chromosome 1 appears to have pleiotropic effects on feed consumption, egg production and behaviour. There was a strong positive correlation between adult body weight and average egg weight. However, three QTLs affecting average egg weight but not body weight were identified. An interesting observation was that the estimated effects for the four major growth QTLs all indicated a codominant inheritance.


In summary:
* 13 loci affected growth (in these White Leghorns)
* 4 of which affected major growth, 50% in females, 80% in males.
* Of these 4 loci, all indicated codominant inheritance.

----------------------------

Further research 2009:
Wahlberg et al. 2009.Genetic analysis of an F2 intercross between two chicken lines divergently selected for body-weight. BMC Genomics. 2009; 10: 248. Full report
This time they refined the research, & included epistatic interactions. Eg, apparently chromosome 7, 'Growth9' QTL is important for expression for other growth loci alleles (including on other autosomal chromosomes).
Quote:
Nine of the 15 unique epistatic pairs involved interaction with the major QTL on chromosome 7 (Growth9)....

....Originally, six genome-wide significant interacting loci were reported on chromosomes 1, 2, 3, 4, 7 and 20. The loci on chromosome 1, 4, 7 and 20 are still genome-wide significant in this analysis, though the loci detected on chromosome 2 and 3 are no longer significant using the new map. On the other hand, two new loci located in a previously uncovered part of chromosome 3 as well as a locus on chromosome 24 now reach significance above the threshold level.



In short - growth factors / body weight is a polygenic trait.

- Growth factor loci were found on chromosomes 1, 2, 3, 4, 7, 20 and 24.

- 15 loci (inc. two new ones) were found to influence growth.

--------------------------------
Another one testing body weight differences between Silkie fowl & White Plymouth Rock:

Gu et al. 2011. Genome-Wide Association Study of Body Weight in Chicken F2 Resource Population PLoS ONE 6(7): e21872. https://doi.org/10.1371/journal.pone.0021872
http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0021872
Quote:
A chicken chromosome 4 (GGA4) region approximately 8.6 Mb in length (71.6–80.2 Mb) had a large number of significant SNP effects for late growth during weeks 7–12. The LIM domain-binding factor 2 (LDB2) gene in this region had the strongest association with body weight for weeks 7–12 and with average daily gain for weeks 6–12. This GGA4 region was previously reported to contain body weight QTL. GGA1 and GGA18 had three SNP effects on body weight with genome-wide significance.

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#116978 - 12/26/17 07:25 PM Re: Journal papers online - reference list [Re: KazJaps]
KazJaps Offline
Classroom Professor

Registered: 08/30/02
Posts: 2871
Loc: Australia
Just released Dec 2017 paper on dwarf chickens, includes research on Seramas, etc:

Wang et al., 2017.
An Evolutionary Genomic Perspective on the Breeding of Dwarf Chickens.
Molecular Biology and Evolution, Volume 34, Issue 12, 1 December 2017, Pages 3081–3088, https://doi.org/10.1093/molbev/msx227
Abstract only
Quote:
Herein, we explore the evolution of the Serama, the smallest breed of chicken. Leveraging comparative population genomics, analyses identify several genes that are potentially associated with the growth and development of bones and muscles. These genes, and in particular both POU1F1 and IGF1, are under strong positive selection. Three allopatric dwarf bantams (Serama, Yuanbao, and Daweishan) with different breeding-histories, form distinct clusters and exhibit unique population structures. Parallel genetic mechanisms underlay their variation in body size. These findings provide insights into the multiple and complex pathways, depending on genomic variation, that chicken can take in response to aviculture selection for dwarfism.

*Unfortunately only the abstract available for free.

-------------------------

Earlier 2017 paper that compares the dwarf Chinese breed Daweishan with a fast growing large breed, the Wuding chicken.

Dou T, Zhao S, Rong H, et al. 2017.
Biological mechanisms discriminating growth rate and adult body weight phenotypes in two Chinese indigenous chicken breeds.
BMC Genomics. 2017;18:469. doi:10.1186/s12864-017-3845-9.
Full Paper

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#116979 - 12/26/17 08:16 PM Re: Journal papers online - reference list [Re: KazJaps]
KazJaps Offline
Classroom Professor

Registered: 08/30/02
Posts: 2871
Loc: Australia
New 2017 Dec. paper on late feathering & ev21:

A Takenouchi, M Toshishige, N Ito, M Tsudzuki; 2017.
Endogenous viral gene ev21 is not responsible for the expression of late feathering in chickens.
Poultry Science, , pex345, https://doi.org/10.3382/ps/pex345
Abstract only
Quote:
Abstract
The late-feathering (LF) gene K on the Z chromosome is an important gene in the chicken industry, which is frequently utilized for the feather sexing, a type of autosexing, of neonatal chicks. The K gene is closely associated with the endogenous ev21 gene from an avian leukosis virus and the incomplete duplication (ID) of prolactin receptor (PRLR) and sperm flagellar protein 2 (SPEF2) genes, and ev21 has been used as a molecular marker to detect LF birds. In the present study, a comprehensive survey for the presence or absence of ev21 and ID across 1,994 birds from 52 chicken breeds, three commercial hybrid groups, and the Red Jungle Fowl revealed that almost all LF breeds have both ev21 and ID. However, only one LF breed (Ingie) has only ID and no ev21. Moreover, this study revealed that almost all early (normal)-feathering (EF) breeds lack both ev21 and ID, but only one breed (White Plymouth Rock) included EF birds with ev21 but no ID. Therefore, regarding LF expression, the results indicated that ID is responsible, but ev21 is not required. Henceforth, ID should be used as a molecular marker to detect LF birds instead of ev21. Because ev21 contains the full genome of an avian leukosis virus, there is a risk of disease development in breeds with this gene. Therefore, the Ingie breed, which has no ev21 at the K locus, represents excellent material for the establishment of new LF stocks.

*Note, earlier research had noted that ev21 positive was not responsible for the late feathering trait, this determined with LF lines where individuals mutated back to wild-type k+ (early feathering) but still ev21 positive. Where the above 2017 research differs is in finding a K late feathering breed that is ev21 negative.

Elferink MG, Vallée AA, Jungerius AP, Crooijmans RP, Groenen MA. 2008.
Partial duplication of the PRLR and SPEF2 genes at the late feathering locus in chicken.
BMC Genomics. 2008;9:391. doi:10.1186/1471-2164-9-391
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2542384/

----------------------

In the following 2016 research paper the authors believed that the SPEF2 gene & not PRLR might be more responsible for the late feathering phenotype (indicated in their gene expression research):

J. Zhao, J. Yao, F. Li, Z. Yang, Z. Sun, L. Qu, K. Wang, Y. Su, A. Zhang, S. A. Montgomery, T. Geng, H. Cui; 2016.
Identification of candidate genes for chicken early- and late-feathering.
Poultry Science, Volume 95, Issue 7, 1 July 2016, Pages 1498–1503, https://doi.org/10.3382/ps/pew131
https://academic.oup.com/ps/article/95/7/1498/2563787
Quote:
Previous studies suggest that prolactin receptor (Prlr) is a potential causative gene for chicken early- (EF) and late-feathering (LF) phenotypes. In this study, we evaluated candidate genes for this trait and determined the expression of 3 genes, including Prlr, sperm flagellar protein 2 (Spef2), and their fusion gene, in the skins of one-day-old EF and LF chicks using RT­qPCR. Data indicated that Prlr expression in the skin did not show significant difference between EF and LF chicks, suggesting Prlr may not be a suitable candidate gene. In contrast, Spef2 expression in the skin displayed a significant difference between EF and LF chicks (P < 0.01), suggesting that Spef2 may be a good candidate gene for chicken feathering. Moreover, dPrlr/dSpef2, the fusion gene, was also a good candidate gene as it was expressed only in LF chicks. However, the expression of the fusion gene was much lower than that of Prlr. Additionally, using strand-specific primers, we found that the fusion gene was transcribed in 2 directions (one from dPrlr promoter, another from dSpef2 promoter), which could result in the formation of a double strand RNA. In conclusion, both Spef2 and the fusion gene are good candidate genes for chicken feathering, but Prlr is not.

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#116985 - 01/07/18 06:16 AM Re: Journal papers online - reference list [Re: KazJaps]
Wieslaw Offline
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Classroom Professor

Registered: 09/18/09
Posts: 3844
Loc: Denmark
Evaluation of genetic resistance to Salmonella Pullorum in three chicken lines.
https://www.ncbi.nlm.nih.gov/pubmed/29294099

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#116986 - 01/07/18 11:51 AM Re: Journal papers online - reference list [Re: Wieslaw]
Wieslaw Offline
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Classroom Professor

Registered: 09/18/09
Posts: 3844
Loc: Denmark
https://www.ncbi.nlm.nih.gov/pubmed/9395470

The chicken genome contains two functional nonallelic beta1,4-galactosyltransferase genes. Chromosomal assignment to syntenic regions tracks fate of the two gene lineages in the human genome.

Abstract
Quote:
Two distinct but related groups of cDNA clones, CKbeta4GT-I and CKbeta4GT-II, have been isolated by screening a chicken hepatoma cDNA library with a bovine beta1,4-galactosyltransferase (beta4GT) cDNA clone. CKbeta4GT-I is predicted to encode a type II transmembrane glycoprotein of 41 kDa with one consensus site for N-linked glycosylation. CKbeta4GT-II is predicted to encode a type II transmembrane glycoprotein of 43 kDa with five potential N-linked glycosylation sites. At the amino acid level, the coding regions of CKbeta4GT-I and CKbeta4GT-II are 52% identical to each other and 62 and 49% identical, respectively, to bovine beta4GT. Despite this divergence in amino acid sequence, high levels of expression of each cDNA in Trichoplusia ni insect cells demonstrate that both CKbeta4GT-I and CKbeta4GT-II encode an alpha-lactalbumin-responsive, UDP-galactose:N-acetylglucosamine beta4-galactosyltransferase. An analysis of CKbeta4GT-I and CKbeta4GT-II genomic clones established that the intron positions within the coding region are conserved when compared with each other, and these positions are identical to the mouse and human beta4GT genes. Thus CKbeta4GT-I and CKbeta4GT-II are the result of the duplication of an ancestral gene and subsequent divergence. CKbeta4GT-I maps to chicken chromosome Z in a region of conserved synteny with the centromeric region of mouse chromosome 4 and human chromosome 9p, where beta4-galactosyltransferase (EC 2.4.1.38) had previously been mapped. Consequently, during the evolution of mammals, it is the CKbeta4GT-I gene lineage that has been recruited for the biosynthesis of lactose. CKbeta4GT-II maps to a region of chicken chromosome 8 that exhibits conserved synteny with human chromosome 1p. An inspection of the current human gene map of expressed sequence tags reveals that there is a gene noted to be highly similar to beta4GT located in this syntenic region on human chromosome 1p. Because both the CKbeta4GT-I and CKbeta4GT-II gene lineages are detectable in mammals, duplication of the ancestral beta4-galactosyltransferase gene occurred over 250 million years ago in an ancestral species common to both mammals and birds.

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#117014 - 02/13/18 01:48 PM Re: Journal papers online - reference list [Re: Wieslaw]
Wieslaw Offline
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Registered: 09/18/09
Posts: 3844
Loc: Denmark
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4805547/

Molecular shifts in limb identity underlie development of feathered feet in two domestic avian species (full paper)


Quote:
Birds display remarkable diversity in the distribution and morphology of scales and feathers on their feet, yet the genetic and developmental mechanisms governing this diversity remain unknown. Domestic pigeons have striking variation in foot feathering within a single species, providing a tractable model to investigate the molecular basis of skin appendage differences. We found that feathered feet in pigeons result from a partial transformation from hindlimb to forelimb identity mediated by cis-regulatory changes in the genes encoding the hindlimb-specific transcription factor Pitx1 and forelimb-specific transcription factor Tbx5. We also found that ectopic expression of Tbx5 is associated with foot feathers in chickens, suggesting similar molecular pathways underlie phenotypic convergence between these two species. These results show how changes in expression of regional patterning genes can generate localized changes in organ fate and morphology, and provide viable molecular mechanisms for diversity in hindlimb scale and feather distribution.


Edited by Wieslaw (02/13/18 01:48 PM)

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#117145 - 04/14/18 12:18 PM Re: Journal papers online - reference list [Re: Wieslaw]
Wieslaw Offline
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Classroom Professor

Registered: 09/18/09
Posts: 3844
Loc: Denmark
Genetics and Genomics of Social Behavior in a Chicken Model.

https://www.ncbi.nlm.nih.gov/pubmed/29531010

Abstract

Quote:
The identification of genes affecting sociality can give insights into the maintenance and development of sociality and personality. In this study, we used the combination of an advanced intercross between wild and domestic chickens with a combined QTL and eQTL genetical genomics approach to identify genes for social reinstatement, a social and anxiety-related behavior. A total of 24 social reinstatement QTL were identified and overlaid with over 600 eQTL obtained from the same birds using hypothalamic tissue. Correlations between overlapping QTL and eQTL indicated 5 strong candidate genes, with the gene TTRAP being strongly significantly correlated with multiple aspects of social reinstatement behavior, as well as possessing a highly significant eQTL.

A link to a free document available.

_____________________________________________________________

Epigenetics and early domestication: differences in hypothalamic DNA methylation between red junglefowl divergently selected for high or low fear of humans.


https://www.ncbi.nlm.nih.gov/pubmed/29609558

Abstract
Quote:
BACKGROUND:
Domestication of animals leads to large phenotypic alterations within a short evolutionary time-period. Such alterations are caused by genomic variations, yet the prevalence of modified traits is higher than expected if they were caused only by classical genetics and mutations. Epigenetic mechanisms may also be important in driving domesticated phenotypes such as behavior traits. Gene expression can be modulated epigenetically by mechanisms such as DNA methylation, resulting in modifications that are not only variable and susceptible to environmental stimuli, but also sometimes transgenerationally stable. To study such mechanisms in early domestication, we used as model two selected lines of red junglefowl (ancestors of modern chickens) that were bred for either high or low fear of humans over five generations, and investigated differences in hypothalamic DNA methylation between the two populations.
RESULTS:
Twenty-two 1-kb windows were differentially methylated between the two selected lines at p&#8201;<&#8201;0.05 after false discovery rate correction. The annotated functions of the genes within these windows indicated epigenetic regulation of metabolic and signaling pathways, which agrees with the changes in gene expression that were previously reported for the same tissue and animals.
CONCLUSIONS:
Our results show that selection for an important domestication-related behavioral trait such as tameness can cause divergent epigenetic patterns within only five generations, and that these changes could have an important role in chicken domestication.


_______________________________________________________________

Genetic and Targeted eQTL Mapping Reveals Strong Candidate Genes Modulating the Stress Response During Chicken Domestication.


https://www.ncbi.nlm.nih.gov/pubmed/27974436
Abstract
Quote:
The stress response has been largely modified in all domesticated animals, offering a strong tool for genetic mapping. In chickens, ancestral Red Junglefowl react stronger both in terms of physiology and behavior to a brief restraint stress than domesticated White Leghorn, demonstrating modified functions of the hypothalamic-pituitary-adrenal (HPA) axis. We mapped quantitative trait loci (QTL) underlying variations in stress-induced hormone levels using 232 birds from the 12th generation of an advanced intercross between White Leghorn and Red Junglefowl, genotyped for 739 genetic markers. Plasma levels of corticosterone, dehydroepiandrosterone (DHEA), and pregnenolone (PREG) were measured using LC-MS/MS in all genotyped birds. Transcription levels of the candidate genes were measured in the adrenal glands or hypothalamus of 88 out of the 232 birds used for hormone assessment. Genes were targeted for expression analysis when they were located in a hormone QTL region and were differentially expressed in the pure breed birds. One genome-wide significant QTL on chromosome 5 and two suggestive QTL together explained 20% of the variance in corticosterone response. Two significant QTL for aldosterone on chromosome 2 and 5 (explaining 19% of the variance), and one QTL for DHEA on chromosome 4 (explaining 5% of the variance), were detected. Orthologous DNA regions to the significant corticosterone QTL have been previously associated with the physiological stress response in other species but, to our knowledge, the underlying gene(s) have not been identified. SERPINA10 had an expression QTL (eQTL) colocalized with the corticosterone QTL on chromosome 5 and PDE1C had an eQTL colocalized with the aldosterone QTL on chromosome 2. Furthermore, in both cases, the expression levels of the genes were correlated with the plasma levels of the hormones. Hence, both these genes are strong putative candidates for the domestication-induced modifications of the stress response in chickens. Improved understanding of the genes associated with HPA-axis reactivity can provide insights into the pathways and mechanisms causing stress-related pathologies.


A link to free document available




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#117146 - 04/14/18 12:43 PM Re: Journal papers online - reference list [Re: Wieslaw]
Wieslaw Offline
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Classroom Professor

Registered: 09/18/09
Posts: 3844
Loc: Denmark
A series of articles on beak deformities:

Study on LOC426217 as a candidate gene for beak deformity in chicken.

https://www.ncbi.nlm.nih.gov/pubmed/26891797



Abstract

Quote:
BACKGROUND:
The beak deformity (crossed beaks) was found in some indigenous chickens of China, such as Beijing-You (BJY), Qingyuan Partridge, and Huxu Chickens. Birds with deformed beaks have reduced feed intake and drinking, impeded growth rate, and poor production performance. Beak deformity reduces the economy of poultry industry and affects animal welfare as well. The genetic basis of this malformation remains incompletely understood. LOC426217, also named claw keratin-like, was the most up-regulated gene in the deformed beaks from a previous digital gene expression (DGE) analysis and was selected as an important candidate gene for further analysis.
RESULTS:
In the present study, quantitative real-time PCR (qRT-PCR) was firstly performed to determine the expression pattern of LOC426217 gene in deformed and normal beaks to verify the DGE results. Tissue-specific expression profile of this gene in 14 tissues was also determined using qRT-PCR. The LOC426217 was amplified from the genomic DNA of 171 deformed and 164 normal beaks, and sequenced to detect the single nucleotide polymorphisms (SNPs). The results showed that LOC426217 was significantly high-expressed in the deformed beaks, which was in good agreement with the DGE results. This gene was specifically high-expressed in beaks than other tissues. Eight SNPs were detected in LOC426217: -62G > T, 24 T > C, 36G > C, 192A > T, 204C > T, 222 T > C, 285G > T, and 363 T > C. Genotype frequency of G-62 T, T24C, G36C, T222C, and T363C loci was significant different between deformed and normal beaks. Haplotype analysis revealed one block with SNPs T24C and G36C, and one block with SNPs A192T, C204T, T222C, and G285T in normal birds, while the block with SNPs G36C and A192T in deformed ones.
CONCLUSIONS:
It was concluded from these results that the over-expression of LOC426217 in the beak maybe related to the malformation. The polymorphisms of LOC426217 gene were associated with the beak deformity trait where the SNPs of G-62 T, T24C, G36C, T222C, and T363C loci maybe used as markers. The specific haplotype block in deformed birds may be a potential linkage marker for this trait.


A link to free document available

_________________________________________________________________

Crossed beaks in a local Swiss chicken breed.


https://www.ncbi.nlm.nih.gov/pubmed/29506524

Abstract

Quote:
BACKGROUND:
Crossed beaks have been reported to occur in Appenzeller Barthuhn, a local Swiss chicken breed. The assumed causes for this beak deformity which are also seen in other bird species including domestic chickens, range from environmental influences to genetic factors. The aim of this project was to characterize the prevalence, the phenotype, and the underlying genetics of crossed beaks in Appenzeller Barthuhn chickens.
RESULTS:
The estimated prevalence of 7% crossed beaks in Appenzeller Barthuhn was significantly higher compared to two other local Swiss chicken breeds. A breeding trial showed significantly higher prevalence of offspring with deformed beaks from mating of affected parents compared to mating of non-affected parents. Examination of 77 Appenzeller Barthuhn chickens with crossed beaks showed a variable phenotype presentation. The deviation of the beak from the median plane through the head ranged from 1° to 61°. In more than 60% of the cases, the upper and lower beak were bent in the same direction, whereas the remaining cases showed different forms of crossed beaks. Computed tomographic scans and bone maceration of the head of two chickens with crossed beaks revealed that the maxilla and the mandibula were affected, while other parts of the skull appeared to be normal. The gene LOC426217, a member of the keratin family, was postulated as a candidate gene for beak deformity in domestic chickens. Sequencing of the coding region revealed two significantly associated synonymous variants for crossed beaks in Appenzeller Barthuhn chickens. A genome-wide association study and a comparative analysis of runs of homozygosity based on high-density SNP array genotyping data of 53 cases and 102 controls showed no evidence of association.
CONCLUSIONS:
The findings suggest a hereditary cause of crossed beaks in Appenzeller Barthuhn chickens. However, the observed variation in the phenotype, together with the inconclusive molecular genetic results indicates the need for additional research to unravel the genetic architecture of this beak deformity.


A link to free document available
________________________________________________________________

Genome-wide detection of CNVs associated with beak deformity in chickens using high-density 600K SNP arrays.

https://www.ncbi.nlm.nih.gov/pubmed/29642269

Quote:
Beak deformity (crossed beaks) is found in several indigenous chicken breeds including Beijing-You studied here. Birds with deformed beaks have reduced feed intake and poor production performance. Recently, copy number variation (CNV) has been examined in many species and is recognized as a source of genetic variation, especially for disease phenotypes. In this study, to unravel the genetic mechanisms underlying beak deformity, we performed genome-wide CNV detection using Affymetrix chicken high-density 600K data on 48 deformed-beak and 48 normal birds using penncnv. As a result, two and eight CNV regions (CNVRs) covering 0.32 and 2.45 Mb respectively on autosomes were identified in deformed-beak and normal birds respectively. Further RT-qPCR studies validated nine of the 10 CNVRs. The ratios of six CNVRs were significantly different between deformed-beak and normal birds (P < 0.01). Within these six regions, three and 21 known genes were identified in deformed-beak and normal birds respectively. Bioinformatics analysis showed that these genes were enriched in six GO terms and one KEGG pathway. Five candidate genes in the CNVRs were further validated using RT-qPCR. The expression of LRIG2 (leucine rich repeats and immunoglobulin like domains 2) was lower in birds with deformed beaks (P < 0.01). Therefore, the LRIG2 gene could be considered a key factor in view of its known functions and its potential roles in beak deformity. Overall, our results will be helpful for future investigations of the genomic structural variations underlying beak deformity in chickens.



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