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3. Dietary iron deficiency compromises normal development of elastic fibers in the aorta and lungs of chicks

Author

Hill, Charles H., Ashwell, Chris M., Nolin, Shelly J., Keeley, Fred, Billingham, Catherine, Hinek, Aleksander, and Starcher, Barry

Subjects
Chicks -- Physiological aspects, Chicks -- Food and nutrition, Chicks -- Genetic aspects, Aorta -- Physiological aspects, Lungs -- Physiological aspects, Animal development -- Chemical properties, Iron deficiency diseases -- Complications and side effects, Iron deficiency diseases -- Physiological aspects, Elastin -- Chemical properties, Elastin -- Physiological aspects, Food/cooking/nutrition
Abstract

Elastic fibers play a key role in the structure and function of numerous organs that require elasticity. Elastogenesis is a complex process in which cells first produce a microfibrillar scaffold, composed of numerous structural proteins, upon which tropoelastin assembles to be cross-linked into polymeric elastin. Recently, it was demonstrated that low concentrations of free iron upregulate elastin gene expression in cultured fibroblasts. The present studies were conducted to assess whether low-iron diets would affect the deposition of elastic fibers in an in vivo model. One-day-old chicks were fed semipurified diets containing 1.3 (low), 12 (moderate), and 24 (control) mg/kg of iron. After 3 wk, chicks in the low-iron group were underweight and anemic. Their aortas were smaller with significantly thinner walls than control chicks, yet elastin or collagen content did not decrease relative to total protein. They also demonstrated a significantly lower stress-strain resistance than the controls. Electron microscopy demonstrated that aortic and lung smooth muscle cells were vacuolated and surrounded by loose extracellular matrix and disorganized elastic lamellae with diffuse and fragmented networks of elastic fibers and microfibrils. Immunohistology demonstrated that fibrillin-3 (FBN3) was disorganized and markedly reduced in amount in aortas of the low-iron chicks. Elastin messenger RNA levels were not downregulated in the tissues from the low-iron-fed chicks; however, there was a significant reduction in expression of the FBN1 and FBN3 genes compared with control chicks. The studies indicate that iron deficiency had a pronounced negative effect on elastic fiber development and suggests that fibrillin may have an important role in this pathology.

Published
2007

9. Genomic Comparison of Indigenous African and Northern European Chickens Reveals Putative Mechanisms of Stress Tolerance Related to Environmental Selection Pressure

Author

Fleming, Damarius S, primary, Weigend, Steffen, additional, Simianer, Henner, additional, Weigend, Annett, additional, Rothschild, Max, additional, Schmidt, Carl, additional, Ashwell, Chris, additional, Persia, Mike, additional, Reecy, James, additional, and Lamont, Susan J, additional

Published
2017
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11. Third Report on Chicken Genes and Chromosomes 2015

Author

Schmid, Michael, Smith, Jacqueline, Burt, David W., Aken, Bronwen L., Antin, Parker B., Archibald, Alan L., Ashwell, Chris, Blackshear, Perry J., Boschiero, Clarissa, Brown, C. Titus, Burgess, Shane C., Cheng, Hans H., Chow, William, Coble, Derrick J., Cooksey, Amanda, Crooijmans, Richard P. M. A., Damas, Joana, Davis, Richard V. N., de Koning, Dirk-Jan, Delany, Mary E., Derrien, Thomas, Desta, Takele T., Dunn, Ian C., Dunn, Matthew, Ellegren, Hans, Eoery, Lel, Erb, Ionas, Farre, Marta, Fasold, Mario, Fleming, Damarius, Flicek, Paul, Fowler, Katie E., Fresard, Laure, Froman, David P., Garceau, Valerie, Gardner, Paul P., Gheyas, Almas A., Griffin, Darren K., Groenen, Martien A. M., Haaf, Thomas, Hanotte, Olivier, Hart, Alan, Haesler, Julien, Hedges, S. Blair, Hertel, Jana, Howe, Kerstin, Hubbard, Allen, Hume, David A., Kaiser, Pete, Kedra, Darek, Kemp, Stephen J., Klopp, Christophe, Kniel, Kalmia E., Kuo, Richard, Lagarrigue, Sandrine, Lamont, Susan J., Larkin, Denis M., Lawal, Raman A., Markland, Sarah M., McCarthy, Fiona, McCormack, Heather A., McPherson, Marla C., Motegi, Akira, Muljo, Stefan A., Muensterberg, Andrea, Nag, Rishi, Nanda, Indrajit, Neuberger, Michael, Nitsche, Anne, Notredame, Cedric, Noyes, Harry, O'Connor, Rebecca, O'Hare, Elizabeth A., Oler, Andrew J., Ommeh, Sheila C., Pais, Helio, Persia, Michael, Pitel, Frederique, Preeyanon, Likit, Barja, Pablo Prieto, Pritchett, Elizabeth M., Rhoads, Douglas D., Robinson, Charmaine M., Romanov, Michael N., Rothschild, Max, Roux, Pierre-Francois, Schmidt, Carl J., Schneider, Alisa-Sophia, Schwartz, Matthew G., Searle, Steve M., Skinner, Michael A., Smith, Craig A., Stadler, Peter F., Steeves, Tammy E., Steinlein, Claus, Sun, Liang, Takata, Minoru, Ulitsky, Igor, Wang, Qing, Wang, Ying, Warren, Wesley C., Wood, Jonathan M. D., Wragg, David, Zhou, Huaijun, Schmid, Michael, Smith, Jacqueline, Burt, David W., Aken, Bronwen L., Antin, Parker B., Archibald, Alan L., Ashwell, Chris, Blackshear, Perry J., Boschiero, Clarissa, Brown, C. Titus, Burgess, Shane C., Cheng, Hans H., Chow, William, Coble, Derrick J., Cooksey, Amanda, Crooijmans, Richard P. M. A., Damas, Joana, Davis, Richard V. N., de Koning, Dirk-Jan, Delany, Mary E., Derrien, Thomas, Desta, Takele T., Dunn, Ian C., Dunn, Matthew, Ellegren, Hans, Eoery, Lel, Erb, Ionas, Farre, Marta, Fasold, Mario, Fleming, Damarius, Flicek, Paul, Fowler, Katie E., Fresard, Laure, Froman, David P., Garceau, Valerie, Gardner, Paul P., Gheyas, Almas A., Griffin, Darren K., Groenen, Martien A. M., Haaf, Thomas, Hanotte, Olivier, Hart, Alan, Haesler, Julien, Hedges, S. Blair, Hertel, Jana, Howe, Kerstin, Hubbard, Allen, Hume, David A., Kaiser, Pete, Kedra, Darek, Kemp, Stephen J., Klopp, Christophe, Kniel, Kalmia E., Kuo, Richard, Lagarrigue, Sandrine, Lamont, Susan J., Larkin, Denis M., Lawal, Raman A., Markland, Sarah M., McCarthy, Fiona, McCormack, Heather A., McPherson, Marla C., Motegi, Akira, Muljo, Stefan A., Muensterberg, Andrea, Nag, Rishi, Nanda, Indrajit, Neuberger, Michael, Nitsche, Anne, Notredame, Cedric, Noyes, Harry, O'Connor, Rebecca, O'Hare, Elizabeth A., Oler, Andrew J., Ommeh, Sheila C., Pais, Helio, Persia, Michael, Pitel, Frederique, Preeyanon, Likit, Barja, Pablo Prieto, Pritchett, Elizabeth M., Rhoads, Douglas D., Robinson, Charmaine M., Romanov, Michael N., Rothschild, Max, Roux, Pierre-Francois, Schmidt, Carl J., Schneider, Alisa-Sophia, Schwartz, Matthew G., Searle, Steve M., Skinner, Michael A., Smith, Craig A., Stadler, Peter F., Steeves, Tammy E., Steinlein, Claus, Sun, Liang, Takata, Minoru, Ulitsky, Igor, Wang, Qing, Wang, Ying, Warren, Wesley C., Wood, Jonathan M. D., Wragg, David, and Zhou, Huaijun

Published
2015
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12. A Genomic Duplication is Associated with Ectopic Eomesodermin Expression in the Embryonic Chicken Comb and Two Duplex-comb Phenotypes

Author

Dorshorst, Ben, Harun-Or-Rashid, Mohammad, Bagherpoor, Alireza Jian, Rubin, Carl-Johan, Ashwell, Chris, Gourichon, David, Tixier-Boichard, Michèle, Hallböök, Finn, Andersson, Leif, Dorshorst, Ben, Harun-Or-Rashid, Mohammad, Bagherpoor, Alireza Jian, Rubin, Carl-Johan, Ashwell, Chris, Gourichon, David, Tixier-Boichard, Michèle, Hallböök, Finn, and Andersson, Leif

Abstract

Duplex-comb (D) is one of three major loci affecting comb morphology in the domestic chicken. Here we show that the two Duplex-comb alleles, V-shaped (D*V) and Buttercup (D*C), are both associated with a 20 Kb tandem duplication containing several conserved putative regulatory elements located 200 Kb upstream of the eomesodermin gene (EOMES). EOMES is a T-box transcription factor that is involved in mesoderm specification during gastrulation. In D*V and D*C chicken embryos we find that EOMES is ectopically expressed in the ectoderm of the comb-developing region as compared to wild-type embryos. The confinement of the ectopic expression of EOMES to the ectoderm is in stark contrast to the causal mechanisms underlying the two other major comb loci in the chicken (Rose-comb and Pea-comb) in which the transcription factors MNR2 and SOX5 are ectopically expressed strictly in the mesenchyme. Interestingly, the causal mutations of all three major comb loci in the chicken are now known to be composed of large-scale structural genomic variants that each result in ectopic expression of transcription factors. The Duplex-comb locus also illustrates the evolution of alleles in domestic animals, which means that alleles evolve by the accumulation of two or more consecutive mutations affecting the phenotype. We do not yet know whether the V-shaped or Buttercup allele correspond to the second mutation that occurred on the haplotype of the original duplication event.

Published
2015
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16. A cis-Regulatory Mutation of PDSS2 Causes Silky-Feather in Chickens

Author

Feng, Chungang, Gao, Yu, Dorshorst, Ben, Song, Chi, Gu, Xiaorong, Li, Qingyuan, Li, Jinxiu, Liu, Tongxin, Rubin, Carl-Johan, Zhao, Yiqiang, Wang, Yanqiang, Fei, Jing, Li, Huifang, Chen, Kuanwei, Qu, Hao, Shu, Dingming, Ashwell, Chris, Da, Yang, Andersson, Leif, Hu, Xiaoxiang, Li, Ning, Feng, Chungang, Gao, Yu, Dorshorst, Ben, Song, Chi, Gu, Xiaorong, Li, Qingyuan, Li, Jinxiu, Liu, Tongxin, Rubin, Carl-Johan, Zhao, Yiqiang, Wang, Yanqiang, Fei, Jing, Li, Huifang, Chen, Kuanwei, Qu, Hao, Shu, Dingming, Ashwell, Chris, Da, Yang, Andersson, Leif, Hu, Xiaoxiang, and Li, Ning

Abstract

Silky-feather has been selected and fixed in some breeds due to its unique appearance. This phenotype is caused by a single recessive gene (hookless, h). Here we map the silky-feather locus to chromosome 3 by linkage analysis and subsequently fine-map it to an 18.9 kb interval using the identical by descent (IBD) method. Further analysis reveals that a C to G transversion located upstream of the prenyl (decaprenyl) diphosphate synthase, subunit 2 (PDSS2) gene is causing silky-feather. All silky-feather birds are homozygous for the G allele. The silky-feather mutation significantly decreases the expression of PDSS2 during feather development in vivo. Consistent with the regulatory effect, the C to G transversion is shown to remarkably reduce PDSS2 promoter activity in vitro. We report a new example of feather structure variation associated with a spontaneous mutation and provide new insight into the PDSS2 function.

Published
2014
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18. A cis-Regulatory Mutation of PDSS2 Causes Silky-Feather in Chickens

Author

Feng, Chungang, primary, Gao, Yu, additional, Dorshorst, Ben, additional, Song, Chi, additional, Gu, Xiaorong, additional, Li, Qingyuan, additional, Li, Jinxiu, additional, Liu, Tongxin, additional, Rubin, Carl-Johan, additional, Zhao, Yiqiang, additional, Wang, Yanqiang, additional, Fei, Jing, additional, Li, Huifang, additional, Chen, Kuanwei, additional, Qu, Hao, additional, Shu, Dingming, additional, Ashwell, Chris, additional, Da, Yang, additional, Andersson, Leif, additional, Hu, Xiaoxiang, additional, and Li, Ning, additional

Published
2014
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20. A Complex Genomic Rearrangement Involving the Endothelin 3 Locus Causes Dermal Hyperpigmentation in the Chicken

Author

Dorshorst, Ben, Molin, Anna-Maja, Rubin, Carl-Johan, Johansson, Anna M., Stromstedt, Lina, Pham, Manh-Hung, Chen, Chih-Feng, Hallböök, Finn, Ashwell, Chris, Andersson, Leif, Dorshorst, Ben, Molin, Anna-Maja, Rubin, Carl-Johan, Johansson, Anna M., Stromstedt, Lina, Pham, Manh-Hung, Chen, Chih-Feng, Hallböök, Finn, Ashwell, Chris, and Andersson, Leif

Abstract

Dermal hyperpigmentation or Fibromelanosis (FM) is one of the few examples of skin pigmentation phenotypes in the chicken, where most other pigmentation variants influence feather color and patterning. The Silkie chicken is the most widespread and well-studied breed displaying this phenotype. The presence of the dominant FM allele results in extensive pigmentation of the dermal layer of skin and the majority of internal connective tissue. Here we identify the causal mutation of FM as an inverted duplication and junction of two genomic regions separated by more than 400 kb in wild-type individuals. One of these duplicated regions contains endothelin 3 (EDN3), a gene with a known role in promoting melanoblast proliferation. We show that EDN3 expression is increased in the developing Silkie embryo during the time in which melanoblasts are migrating, and elevated levels of expression are maintained in the adult skin tissue. We have examined four different chicken breeds from both Asia and Europe displaying dermal hyperpigmentation and conclude that the same structural variant underlies this phenotype in all chicken breeds. This complex genomic rearrangement causing a specific monogenic trait in the chicken illustrates how novel mutations with major phenotypic effects have been reused during breed formation in domestic animals.

Published
2011
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24. A cis-Regulatory Mutation of PDSS2 Causes Silky-Feather in Chickens.

Author

Feng, Chungang, Gao, Yu, Dorshorst, Ben, Song, Chi, Gu, Xiaorong, Li, Qingyuan, Li, Jinxiu, Liu, Tongxin, Rubin, Carl-Johan, Zhao, Yiqiang, Wang, Yanqiang, Fei, Jing, Li, Huifang, Chen, Kuanwei, Qu, Hao, Shu, Dingming, Ashwell, Chris, Da, Yang, Andersson, Leif, and Hu, Xiaoxiang

Subjects
CHICKEN breeds, ANIMAL genetics, CHICKENS, CHROMOSOMES, ALLELES, GENETIC mutation
Abstract

Silky-feather has been selected and fixed in some breeds due to its unique appearance. This phenotype is caused by a single recessive gene (hookless, h). Here we map the silky-feather locus to chromosome 3 by linkage analysis and subsequently fine-map it to an 18.9 kb interval using the identical by descent (IBD) method. Further analysis reveals that a C to G transversion located upstream of the prenyl (decaprenyl) diphosphate synthase, subunit 2 (PDSS2) gene is causing silky-feather. All silky-feather birds are homozygous for the G allele. The silky-feather mutation significantly decreases the expression of PDSS2 during feather development in vivo. Consistent with the regulatory effect, the C to G transversion is shown to remarkably reduce PDSS2 promoter activity in vitro. We report a new example of feather structure variation associated with a spontaneous mutation and provide new insight into the PDSS2 function. [ABSTRACT FROM AUTHOR]

Published
2014
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25. Genomic Comparison of Indigenous African and Northern European Chickens Reveals Putative Mechanisms of Stress Tolerance Related to Environmental Selection Pressure.

Author

Fleming DS, Weigend S, Simianer H, Weigend A, Rothschild M, Schmidt C, Ashwell C, Persia M, Reecy J, and Lamont SJ

Subjects
Animals, Chickens physiology, Haplotypes, Homozygote, Polymorphism, Genetic, Chickens genetics, Environment, Genome, Selection, Genetic, Stress, Physiological genetics
Abstract

Global climate change is increasing the magnitude of environmental stressors, such as temperature, pathogens, and drought, that limit the survivability and sustainability of livestock production. Poultry production and its expansion is dependent upon robust animals that are able to cope with stressors in multiple environments. Understanding the genetic strategies that indigenous, noncommercial breeds have evolved to survive in their environment could help to elucidate molecular mechanisms underlying biological traits of environmental adaptation. We examined poultry from diverse breeds and climates of Africa and Northern Europe for selection signatures that have allowed them to adapt to their indigenous environments. Selection signatures were studied using a combination of population genomic methods that employed F ST , integrated haplotype score (iHS), and runs of homozygosity (ROH) procedures. All the analyses indicated differences in environment as a driver of selective pressure in both groups of populations. The analyses revealed unique differences in the genomic regions under selection pressure from the environment for each population. The African chickens showed stronger selection toward stress signaling and angiogenesis, while the Northern European chickens showed more selection pressure toward processes related to energy homeostasis. The results suggest that chromosomes 2 and 27 are the most diverged between populations and the most selected upon within the African (chromosome 27) and Northern European (chromosome 2) birds. Examination of the divergent populations has provided new insight into genes under possible selection related to tolerance of a population's indigenous environment that may be baselines for examining the genomic contribution to tolerance adaptions., (Copyright © 2017 Fleming et al.)

Published
2017
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