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[分享] 亚洲猪如何进入欧洲的论文

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发表于 2019-2-8 01:33 | 显示全部楼层 |阅读模式
亚洲猪如何进入欧洲的论文。

Historical records and molecular evidence indicate that Asian pigs were introduced into Europe during the 18th and early 19th centuries (Giuffra et al., 2000; Kijas et al., 2001a). https://pdfs.semanticscholar.org/3af8/77065f3313f6150e0f64252c4a8a30afdf9b.pdf
Giuffra, E., Evans, G., Tornsten, A., Wales, R., Day, A., Looft, H., Plastow, G. & Andersson, L. 1999. The Belt mutation in pigs is an allele at the Dominant white (I/KIT) locus. Mammalian Genome 10, 1132-1136.
Giuffra, E., Kijas, J.M., Amarger, V., Carlborg, O., Jeon, J.T. & Andersson, L. 2000. The origin of the domestic pig: independent domestication and subsequent introgression. Genetics 154, 1785-1791.
Pig coat colour genetics Domestication of pigs has occurred independently from Wild Boar subspecies in Europe and Asia. Historical records and molecular evidence indicate that Asian pigs were introduced into Europe during the 18th and early 19th centuries (Giuffra et al., 2000; Kijas et al., 2001a). There are several varieties of coat colour phenotypes in domesticated pigs. Most of the European breeds, such as Large White and the different Landrace pigs have a white coat colour, while the uniform black coat is the most common type in breeds from China (Legault, 1998). The main genes in pig coat colour genetics, controlling the relative amounts of melanin, eumelanin (black/brown) and phaeomelanin (yellow/red), have also been identified as the extension and agouti loci. In a variety of mammals, dominant alleles at the extension act to produce uniform black coat colour, whereas recessive alleles at this locus extend the amount of red/yellow pigment. Dominant alleles at the agouti, on the other hand, cause a yellow coat whereas the homozygosity for the bottom recessive allele is associated with a uniform black coat (Jackson, 1997). The uniform black colour in pigs is caused by mutations in the extension locus, probably resulting in constitutively active melanocortin receptor 1 (Kijas et al., 1998). There are other MC1R alleles associated with wild-type, black spotting and uniform red coat colour, the latter being probably caused by a disruption of MC1R function (Kijas et al., 1998; Kijas et al., 2001b). Several additional loci affecting coat colour in pigs have been mapped recently by whole-genome scan (Hirooka et al., 2002). During this study additional loci affecting white and black phenotypes were located, one of them possibly representing the porcine equivalent to the KIT ligand called MGF. Dominant white coat colour in pigs Already in 1906, Spillman concluded that the white coat colour in domestic pigs is a dominant trait. Since then, the potential cause for white coat in domestic pigs has been unravelled primarily using an intercross between Large White (I/I) and Wild Boar (i/i) pigs, carried out in Uppsala. First it was shown that the responsible gene is located on pig chromosome 8 and KIT gene was proposed as a potential candidate gene (Johansson et al., 1992). KIT encodes a mast/stem cell growth factor receptor, a key signal-transducing receptor in stem cell systems feeding into multiple lineages such as haematopoietic cells, germ cells, melanocytes, intestinal pacemaker cells and neuronal cells (reviewed in Bernstein et al., 1990; Broudy, 1997). Therefore, the dominant white phenotype in pigs, being due to a mutation in KIT that leads to lack of melanocytes in the skin, is consistent. Mutations in this gene also cause pigmentation disorders in mice, called Dominant white spotting/W (Chabot et al., 1988; Geissler, Ryan & Housman, 1988), and in humans, called piebald trait (Fleischman et al., 1991; Giebel & Spritz, 1991). In the mouse, loss-of-function mutations are associated with limited white spotting in heterozygotes, but they are often lethal or sublethal in the homozygous condition due to their effects on haematopoiesis (Fleischman & Mintz, 1979; Waskow et al., 2002). 10 In 1996 Johansson Moller and others presented genetic data demonstrating that the KIT gene in white pigs is duplicated. Furthermore, in 1998, the cause for dominant white phenotype in pigs was being presented as two mutations in the KIT gene – one gene duplication associated with a partially dominant phenotype and a splice mutation in one of the copies, leading to the fully dominant allele (Marklund et al., 1998). The splice mutation is a G to A substitution in the first nucleotide of intron 17 leading to skipping of exon 17. Exon 17 is composed of 123 bp and the mutation is thus an in-frame mutation deleting 41 amino acids from the protein. Those 41 amino acids are part of a highly conserved region in tyrosine kinases, comprising the catalytic loop and part of the activation loop (Hubbard et al., 1994). In contrast to the duplication, considered to be a regulatory mutation, the splice mutation is expected to cause a receptor with impaired or absent tyrosine kinase activity. But on the other hand, the existence of KIT duplication in domestic pigs allows the expression of at least one normal KIT receptor per chromosome, which is apparently sufficient to avoid severe pleiotropic effects on the tissues. Another common phenotype in domesticated pigs, associated with KIT locus, is a white belt. It is a dominant phenotype and may occur against a solid black (Hampshire) or red background (Bavarian Landschwein). Many mouse mutants display a white belt of variable width and position across the body, for instance patch and rump-white. It is known that patched phenotype in mice is caused by a deletion located ~180 kb upstream of KIT gene and rump-white is caused by a large inversion involving the same region. In pigs, the locus responsible for belted phenotype has been mapped to chromosome 8, which harbours the KIT gene. Therefore, the belt mutation is probably caused by a regulatory mutation affecting KIT expression (Giuffra et al., 1999). Gene duplications in mammalian genomes Large segmental duplications are very common in mammalian genomes. These duplications are abundant (5% of the genome), span large genomic distances (1- 100 kb) and can have very high sequence identity (95-100%) (Eichler, 2001; Bailey et al., 2002). The high level of sequence identity provides an ample substrate for recombination events. Furthermore, nearly identical sequence copies in the genome created by duplications may lead to large-scale chromosomal rearrangements, such as deletions, inversions, translocations and additional duplications. The duplications can harbour large pieces of genetic material and contain both high-copy number repeats and gene sequences with exon-intron structures. An important feature of duplications is that if they harbour coding sequences, they may not include the whole coding region and regulatory elements of a gene. It has become apparent though, that many duplicated segments are expressed, although the transcripts frequently show tissue specific transcription pattern (germline, fetal, cancerous), contain premature stop codons and are non-functional (Horvath et al., 2001). Several of such transcripts are chimeric, incorporating exons from different 11 genes, which raises the possibility of a mechanism akin to exon shuffling. Therefore, such chromosomal rearrangements as duplications are considered as exclusive contributors to the origin of reproductive isolation and the formation of new species (Lynch, 2002). Moreover, it has been proposed that imprinting may originally have evolved on a simple basis of dosage compensation required for some duplicated genes or chromosomes (Walter & Paulsen, 2003). This indicates that duplications may play an even more important role in the development of genomes than just gene innovation and speciation. The distribution of duplication events on human chromosomes seems nonuniform and detailed analysis has revealed that larger blocks of duplicated material are, in fact, composed of smaller units of modules of duplications. There are several potential explanations to duplications being more abundant in subtelomeric and perisentromeric regions. One of them relies on their lower gene density, showing a greater tolerance of these regions for the incorporation of new genetic material without adverse effects to the organism. However, there are other parts of chromosomes that are devoid of genes and yet show no increase in segmental duplication (Horvath et al., 2001). Another explanation to duplicated segments being positioned near centromeres could be a simple suppression of recombination in this region, resulting in a slower deletion of new genetic material. Segmental duplications in human have been indicated as one type of chromosomal rearrangements causing genetic diseases. It has been estimated that 1 in every 1000 human births has a duplication-mediated germline rearrangement. For instance, human cytochromes and chemokines are known to have interindividual and interethnic variabilities in copy numbers. Since cytochromes are enzymes involved in metabolism of endogenous and exogenous compounds, the variability in copy number leads to differences in effects and toxicities of many drugs (antidepressants, neuroleptics, cardiovascular agents, etc.) and environmental compounds (nicotine, etc.) (Xu et al., 2002; Lovlie et al., 1996; Johansson et al., 1996). Differences in copy number of chemokines are likely to affect responses to infection, and influence the cause of autoimmune and inflammatory diseases, as well as alter the patient reaction to treatment (Townson, Barcellos & Nibbs, 2002). Therefore, an established fast and easy-to-use method for analysis of gene copy numbers is of major interest.



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