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#116930 - 11/29/17 06:40 AM Re: Avian leucosis, Marek's & other diseases [Re: Redcap]
Wieslaw Offline
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Registered: 09/18/09
Posts: 3831
Loc: Denmark
Here is an exciting article:
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5356597/

GADD45&#946;, an anti-tumor gene, inhibits avian leukosis virus subgroup J replication in chickens

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#116980 - 12/26/17 08:23 PM Re: Avian leucosis, Marek's & other diseases [Re: Wieslaw]
KazJaps Offline
Classroom Professor

Registered: 08/30/02
Posts: 2864
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/

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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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#116984 - 01/07/18 06:14 AM Re: Avian leucosis, Marek's & other diseases [Re: KazJaps]
Wieslaw Offline
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Registered: 09/18/09
Posts: 3831
Loc: Denmark
Evaluation of genetic resistance to Salmonella Pullorum in three chicken lines.

https://www.ncbi.nlm.nih.gov/pubmed/29294099

Abstract:
Quote:
Resistance to diseases varies considerably among populations of the same species and can be ascribed to both genetic and environmental factors. Salmonella Pullorum (SP) is responsible for significant losses in the poultry industry, especially in developing countries. To better understand SP resistance in chicken populations with different genetic backgrounds, we orally challenged 3 chicken lines with SP-a highly selected commercial breed (Rhode Island Red, RIR), a local Chinese chicken (Beijing You, BY), and a synthetic layer line (dwarf, DW)-at 4 d of age. Two traits related to SP resistance, survival, and bacterial carriage in the spleen were evaluated after infection. Survival rates were recorded up to 40 d of age when all chickens still alive were killed to verify the presence of SP in the spleen to determine carrier state. Mortalities for RIR, BY, and DW chicks were 25.1%, 8.3%, and 22.7%, respectively, and the corresponding carrier-states in the spleens were 17.9%, 0.6%, and 15.8%. Survival and carrier-state heritabilities were estimated using an animal threshold model. Survival heritability was 0.197, 0.091, and 0.167 in RIR, BY, and DW populations, respectively, and the heritabilities of carrier state for DW and RIR were 0.32 and 0.16, respectively. This is the first time that the heritability of the SP carrier state has been evaluated in chickens. Our study provides experimental evidence that chickens with various genetic background exhibited significantly different SP-resistant activities and heritabilities. These results may be useful for selecting lines with better disease resistance.

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#116996 - 01/21/18 03:49 PM Re: Avian leucosis, Marek's & other diseases [Re: Wieslaw]
Wieslaw Offline
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Registered: 09/18/09
Posts: 3831
Loc: Denmark
Naturally Occurring Frame-Shift Mutations in the tvb Receptor Gene Are Responsible for Decreased Susceptibility of Chicken to Infection with Avian Leukosis Virus Subgroups B, D, and E.

https://www.ncbi.nlm.nih.gov/pubmed/29263268

Abstract:

Quote:
The group of highly related avian leucosis viruses (ALVs) in chickens thought to have evolved from a common retroviral ancestor into six subgroups, A to E and J. These ALV subgroups use diverse cellular proteins encoded by four genetic loci in chickens as receptors to gain entry into host cells. Host exposed to ALVs might be under selective pressure to develop resistance to ALVs infection. Indeed, the resistant alleles have previously been identified in all four receptor loci in chicken. The tvb gene encodes a receptor, which determines the susceptibility of host cells to the subgroups B, D, and E ALV. We herein describe the identification of two novel alleles of tvb receptor gene, which possess independent insertions each within the exon 4. The insertions resulted in frame-shift mutations reveal a premature stop codon that causes nonsense-mediated decay of the mutant messenger RNA, and the production of truncated Tvb protein. As a result, we observed that the frame-shift mutations in the tvb gene significantly lower the binding affinity of the truncated Tvb receptors for the ALV-B, ALV-D and ALV-E envelope glycoproteins, and significantly reduce susceptibility to infection by ALV-B, ALV-D and ALV-E in vitro and in vivo Taken together, these findings are suggestive for frame-shift mutation can be a molecular mechanism of reduction of susceptibility to ALV and enhance our understanding of virus-host coevolution.IMPORTANCE Avian leukosis virus (ALV) once caused devastated economic loss to the U.S. poultry industry prior the current eradication schemes in place, and continues causing severe calamity to the poultry industry in China and Southeast Asia, where deployment of a complete eradication scheme remains a challenge. The tvb gene encodes the cellular receptor necessary for the subgroup B, D, and E ALV infection. Two tvb allelic variants resulted from frame-shift mutations have been identified in this study, which have been elucidated with significantly reduced functionality in mediating the subgroups B, D, and E ALV infection. Unlike the control of herpesvirus-induced diseases by vaccination, the control of avian leukosis in chickens has been totally relying on virus eradication measures and host genetic resistance. This finding enriches the allelic pool of tvb gene, and expands the potentiality for genetic improvement of ALV resistance in varied chicken populations by selection.

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Acquisition of resistance to avian leukosis virus subgroup B through mutations on tvb cysteine-rich domains in DF-1 chicken fibroblasts.

https://www.ncbi.nlm.nih.gov/pubmed/28903753

Abstract:


Quote:
Avian leukosis virus (ALV) is a retrovirus that causes tumors in avian species, and its vertical and horizontal transmission in poultry flocks results in enormous economic losses. Despite the discovery of specific host receptors, there have been few reports on the modulation of viral susceptibility via genetic modification. We therefore engineered acquired resistance to ALV subgroup B using CRISPR/Cas9-mediated genome editing technology in DF-1 chicken fibroblasts. Using this method, we efficiently modified the tumor virus locus B (tvb) gene, encoding the TVB receptor, which is essential for ALV subgroup B entry into host cells. By expanding individual DF-1 clones, we established that artificially generated premature stop codons in the cysteine-rich domain (CRD) of TVB receptor confer resistance to ALV subgroup B. Furthermore, we found that a cysteine residue (C80) of CRD2 plays a crucial role in ALV subgroup B entry. These results suggest that CRISPR/Cas9-mediated genome editing can be used to efficiently modify avian cells and establish novel chicken cell lines with resistance to viral infection.


Edited by Wieslaw (01/21/18 03:52 PM)

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#116997 - 01/23/18 02:54 PM Re: Avian leucosis, Marek's & other diseases [Re: Wieslaw]
Wieslaw Offline
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Classroom Professor

Registered: 09/18/09
Posts: 3831
Loc: Denmark

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#117024 - 02/20/18 11:40 AM Re: Avian leucosis, Marek's & other diseases [Re: Wieslaw]
Redcap Offline
Ruler of the Roost

Registered: 08/14/06
Posts: 985
Loc: Germany
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