绵羊Leptin基因与部分经济性状的遗传相关性研究
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摘要
本研究以蒙古羊、滩羊、小尾寒羊和欧拉型藏羊为研究对象,选取瘦素蛋白基因(Leptin)作为候选基因,利用6个位点对其进行遗传多样性研究,同时研究其作为候选基因对生产性状进行分子标记的可行性,得到如下结果:
     1.根据已公布的绵羊Leptin基因序列,分别在第三外显子,第二内含子和3’非翻译区筛选6个位点设计引物,并进行PCR扩增,均得到了特异性扩增结果。经检测L1、L2、L3和L4,4个位点存在多态性,均为三个基因型AA、AB和BB型,其中AA型为野生型,AB型为杂合子,BB型为突变基因型。L1位点BB型在404bp处有一突变,为G—A突变; L2位点BB型在103bp处有一突变,为G—T突变; L3位点BB型在162bp处有一突变,为A—G突变; L4位点BB型在268bp处有一突变,为G—A突变;4个群体在4个位点上的有效等位基因数小于实际观察等位基因数。
     2.本试验对4个多态位点进行基因频率卡方检验,发现L1位点只有在小尾寒羊群体处于Hardy-Weinberg平衡状态;L2和L4位点在蒙古羊和滩羊群体处于Hardy-Weinberg平衡状态;L3位点只有在欧拉羊群体处于Hardy-Weinberg不平衡状态。4个群体的平均有效等位基因数为1.7162,与实际观察值相近,说明等位基因数分布较均衡。L1、L3和L4三个位点在蒙古羊群体的多态信息含量和信息熵均大于其他3个品种群体,证明了蒙古羊具有丰富的遗传基础。L2位点在滩羊群体的多态信息含量最大,说明滩羊的该位点遗传基础丰富。
     3.将4个含有多态基因型的位点与4个品种绵羊的部分经济性状进行相关性分析结果如下:
     在蒙古羊群体中,L1位点与屠宰率存在相关性,各基因型的均值差异显著(P<0.05);L2位点与背膘厚、体重和胴体重存在相关性,但各基因型的均值差异显著(P<0.05),可作为蒙古羊活重等6个屠宰性状的标记位点,其中L2-AA型所对应活重、胴体重、背膘厚、花油重和腹脂重的最小二乘均数皆为最大,且与其他两个基因型比较,差异显著(P<0.05),可作为蒙古羊的活重等5个性状的标记基因型;L3位点只与屠宰率存在相关性,且各基因型的均值差异显著(P<0.05),对L3位点和L1位点选择效应比较得知,L3-BB基因型可作为蒙古羊群体的屠宰率标记基因型;L4位点与屠宰率存在相关性,且各基因型的均值差异显著(P<0.05)。
     在小尾寒羊群体中,L1位点多态性与背膘厚存在相关性,各基因型的均值差异显著(P<0.05);L3位点多态性与体重、胴体重、背膘厚、肾脏脂肪重、花油重和腹脂重存在相关性,各基因型的均值差异极显著(P<0.01),且L3-BB基因型的最小二乘均值最大,可作为胴体重、肾脏脂肪重和腹脂重的标记基因型,此外对L3位点和L4位点选择效应比较得知,L3-BB基因型也可作为小尾寒羊群体的体重和背膘厚标记基因型;L4位点多态性与小尾寒羊的体重和背膘厚存在相关性,各基因型的均值差异极显著(P<0.05)。
     在滩羊群体中,L3位点多态性与体重、胴体重和花油重存在相关性,且各基因型均值差异显著(P<0.05),其中L3-BB基因型对应最小二乘均值最大,可作为滩羊的体重、胴体重和花油重的标记基因型;
     在欧拉羊群体中,L1位点与体重有相关性,且各基因型的均值差异显著(P<0.05);L2位点与体重有相关性,且各基因型的均值差异显著(P<0.05);L3位点与体重有相关性,且各基因型的均值差异显著(P<0.05)对L3位点与L1和L2位点选择效应比较得知,L3-BB基因型也可作为欧拉羊群体的体重标记基因型。
Mongolian sheep, Tan sheep, Small-Tail Han sheep and Ola Tibet sheep were used as research populations. The DNA molecular marker technologies PCR-SSCP were applied to evaluate the effects of genotypes of the candidate gene-leptin gene on carcass traits in the populations. The Association between genetic marker and the carcass traits, including the weight, carcass weight, renal adipose weight, celiac adipose weight, alvine adipose weight,dressing percentage,GR value,backfat thickness were analyzed using general linear model (GLM). The results were as follows:
     1.Based on the sequence of the goat leptin gene, six primers were designed, which included the exon3, intron2 and 3’UTR. The results showed that four loci were demonstrated polymorphism in the six selected locus in tested population. The genotypes were nominated AA, AB, and BB. And the AA genotype was wild type while the AB was heterozygote, the BB was mutation type.
     The sequencing results revealed that in the L1 locus, a G>A mutation at the 404th nucleotide; in the L2 locus, a G>T mutation was detected at the 103th nucleotide; in the L3 locus, an A>G mutation was found at the 162th nucleotide; in the L4 locus, a G>A mutation was found at the 268th nucleotide. In the tested population, the effective allele number was smaller than the observed allele number.
     2.The frequencies of the four loci were analyzed usedλ-test. The results revealed that at the L1 locus the Small-Tail Han sheep was at Hardy-Weinberg equilibrium; at the L2 and L4 loci the Mongolian sheep and Tan sheep were at Hardy-Weinberg equilibrium; at the L3 locus only the Ola Type Tibet sheep was at Hardy-Weinberg equilibrium. The average effective allele number was 1.7162 which was similar to the observed allele number and this implied that the distributions of the alleles were equilibrium in the four breeds. The PIC and Shannon’s information index(S) were higher in the Mongolian sheep than other breeds at the L1, L3 and L4 locus, and this suggested that the Mongolian sheep contained genetic diversity. At the L2 loci, the PIC was much higher than other breeds, it revealed that genetic diversity were ample in this locus.
     The association of variations of leptin gene with carcass traits in the population was analyzed. The results were showed as followe:
     3.In the Mongolian sheep, the genotype of the L1 locus was associated with the dressing percentage,and the relationship was significant(P<0.05); However, there was significant association between the genotype of the L2 locus and the backfat thickness、body weight and carcass weight(P<0.05), which can be used a maker of the carcass trait. The least-squares analysis showed that the body weight、carcass trait、backfat thickness、dressing percentage and celiac adipose weight of individuals , which was the L2-AA, were higher than the other which were the other two genotypes, and this suggested that the locus can be used as a maker of the traits. There was significant association between the genotype of the L3 locus and the dressing percentage(P<0.05).
     L3-BB can be used a maker of the carcass traits through comparing the selected effects of the L1 and L3. L4 was also associated with the dressing percentage(P<0.05). In the Small-Tail Han sheep population, there were significant relationship between the genotype of the L1 and the backfat thickness (P<0.05). and there were significant association between the genotype of the L3 and the body weight、carcass weight、backfat thickness、renal adipose weight、dressing percentage和celiac adipose weight (P<0.01). The least-squares analysis showed that the body weight、carcass weight、backfat thickness、dressing percentage andceliac adipose weight of individuals, which was the L3-BB, were the highest than the others which were the other two genotypes, and this suggested that the locus can be used as a maker of carcass weight、renal adipose weight and celiac adipose weight traits. L3-BB can be used a maker of the carcass traits through comparing the selected effects of the L3 and L4. the polymorphism of the L4 locus was also associated with the body weight and backfat thickness(P<0.05).
     In the Tan sheep population, there was a significant relationship between the genotype of the L3 locus and the body weight, carcass weight and dressing percentage. The least-squares analysis showed that the L3 locus can be used a maker of the body weight、carcass weight and dressing percentage.
     In the Ola Tibet sheep population, there was a significant relationship between the genotype of the L1 and the body weight (P<0.05), as well as the L2 and L3 (P<0.05). L3-BB can be used a maker of the body weight through comparing the selected effects of the L1 and L2.
引文
[1] 田野.高级运动生理学教程[M].北京:高等教育出版社,2003:766-794
    [2] 林季.颜光涛.Leptin 与内毒素[J].标记免疫分析.2004(11):41-45
    [3] Kennedy GC. Thc role of depot fat in hypothalamic control of food in the rat. Proceedings RoyalSociety Version B,1953;140:578-59220
    [4] Coleman DL.Obese and diatbetes:two mutant genes causing diabecles-obesity syndrome in mice.Diabetoloeia,1978;14:141-148.
    [5] Zhan Y,Proenca R,Maffei M,et a1.Positional cloning of the mouse obese gene and its human homologous.Naturc,1994;372:425—432
    [6] Montague CT, Farooqi IS,Whitehead JP, et al.Congenital Leptin deficiency is associated with early-onset obesity in humans.Nature,1997;903-908
    [7] Kopecky J. Expression of the mitochondrial uncoupling protein gene from the ap2 gene promoter prevents genetic obesity. J Clin Invest, 1995,96:2914.
    [8] Zhang Y,Proenca R,Maffei M,et al.Positional cloning of the mouse obese gene and its human homologue(Erratum Nature 1995,374:479),Nature,1994,372:425-432.
    [9] Green ED, Maffei M,Braden VV. The human obese (OB) gene:RNA expression pattern and mapping on the physical,cytogenetic, and genetic maps of chromosome 7.Genome Res. 1995 Aug,5(1):5-12.
    [10] Cohen SL, Halaas JL, Friedman JM, et al. Human Leptin characterization. Nature,1996,382:589
    [11] Song WC,Moore R,et al.Molecular characterization of a testis-specific estrogen sulfotransferase and aberrant liver expression in obese and diabetogenic C57BL/KsJ- db/ db mice. Endocrin,1995,136 (6):2477-2484.
    [12] Bado A, Levasseur S, Attoub S, et al.The stomach is a source of Leptin.Nature, 1998, 394:790-793.
    [13] Henson MC, Swan KF, O’Neil,JS.Expression of placental Leptin and Leptin receptor transcripts in early pregnancy and at term. Obstet Gynecol 1998, 92:1020-1028.
    [14] Umemoto Y, Tsuji K, Yang FC, et al. Leptin stimulates the proliferation of murine myelocytic and primitive hematopoietic progenitor cells.Blood,1997, 90:3438 一 43.
    [15] Estienne MJ, Harper AF, Barb CR, et al.Concentrations of Leptin in serum and milk collected from lactating sows differing in body condition.Domestic Animal Endocrinology,2000,19:275-280.
    [16] Bidwell CA, Ji S, Frank GR, et al.Cloning and expression of the porcine obese gene. Animal Biotechnology, 1997, 8(2),191 一 206
    [17] Lopez-Soriano J, Carbo N, Lopez Soriano F. J. et al.,Leptin levels and gene expression duing the perinatal phase in the rat. Eur J obesity Gynecol Reprod Biol, 1998, 81(1):95-100
    [18] Rock F L.et al.The Leptin haemopoietic cytoline fold is stabilized by intrachain disfufide bond. Norm. Metab. Res, 1996, 28:648-652.
    [19] Keisler DH, Daniel JA, Morrison CD. The role of Leptin in nutritional status and reproductive function. J Reprod Fertil Suppl, 1999;54:425-435.
    [20] Campfield LA, Smith FJ, Guisez Y, et al.Recombinant mouse OB protein: Evidence for a peripheral signal linking adiposity and central neural networks. Science, 1995, 269:546-549.
    [21] Maffei M, Halaas J, Ravussin E,et al. Leptin levels in human and rodent: measurement of plasma Leptin and ob RNA in obese and weight 一 reduced subjects. Nature Med,1995,1:1155-1161.
    [22] Frederich RC, Hamann A, Anderson S, et al. Leptin levels reflect body lipid content in mice: Evidence for diet 一 induced resistance to Leptin action, Nature Med, 1995a, 1:1311 一 1314.
    [23] Considine RV, Sinha MK, Heiman ML, et al.Serum immunoreactive-Leptin concentration in normal-weight and obese humans. N Engl J Med,1996b,334:292——95.
    [24] Houseknecht KL, Flier SN,Frederich RC, et al.Secretion of Leptin and TNF- a by the adipocyte vitro:Regulation with genetic and dietary induced obesity(Abstr.).J.Anim. Sci.1996a,74 (Suppl. 1):81.
    [25] Moinat M, Deng C, Muzzin P, et al.Modulation of obese gene expression in rat brown and white adipose tissues. FEBS Lett, 1995, 373:131 一 134.
    [26] Cusin I et al.The ob gene and insulin A relationship leading to clues to the understanding of obesity. Diabetes, 1995, 44:1467-1470
    [27] Frederich RC, Lollmann B, Napolitano- Rosen A, et al. Expression of ob mRNA and its encoded protein in rodents, Impact of nutrition and obesity. J. Clin. Invest, 1995b, 96:1658-1663.
    [28] Trayhurn P,Thomas MEA, Duncan JS, et al.Effects of fasting and refeeding on ob gene expression in white adipose tissue of lean and obese mice. FEBS Lett, 1995, 368:488-490.
    [29] Kolaczynski JW, Considine RV, Ohannesian J, et al. Responses to Leptin in short 一 term fasting and refeeding in humans:a link with ketogenesis but not ketones themselves. Diabetes 1996a,45:1511 一1515.
    [30] Spinedi E, Gaillard RC. A regulatory loop between the hypothalamo-pituitary-adrena(lHPA) axis and circulating Leptin:a physiological role of ACTH. Endocrinology,1998, 139:4016-4020.
    [31] Stephens T. W.,M. Basinski,P. K. Bristow, et al. The role of neuropeptideY in the anti-obesity action of the obese gene product.Nature, 1995,377: 530-532.
    [32] Spiegelman BM and Filert JS. Obesity and the regulation of energy balance. Cell,2001 104:531 一543.
    [33] Pelleymounter MA, Cullen MJ, Baker MB,et al. Effects of the obese gene product on body weight regulation in ob/ob mice. Science, 1995, 269:540-543.
    [34] Halaas JL, Gagiwala KS, Maffei M. et al.Weight-reducing effects of the plasma protein encoded by the obese gene. Science, 1995,269:543-546.
    [35] Barb CR, YanX, Azain MJ, et al. Recombinant porcine Leptin reduces feed intake and stimulates growth hormone secretion in swine. Dourest Anim Endocrinol 1998, 15:77-86.
    [36] Masuzaki H, Ogawa Y, Isse N,et al.Human obese gene expression adipocyte-specific expression and regional differences in the adipocyte tissue. Diabetes, l995,44:855-858.
    [37] Devaskar SU, Ollesch C, Rajakumar RA, et al.Developmental changes in ob gene expression and circulating Leptin peptide concentrations. Biochem Biophys Res Commun, 1997, 238(1):44-47.
    [38] Sparks RL, Allen BJ, Strauss EE, et al.TGF-βblocks early but not late differentiation-specific gene expression and morphologic differenttiation of 3T3T preadipocytes.J Cell Physiol 1992,150:568-577.
    [39] Inoue S, et al.Transplantation of pancreatic bate cells prevents the development of hypothalamic obesity in rats. American Journal of Physiology, 1978, 235:266-271.
    [40] Dallman MF, et al.The neutral network that regulates energy balance is responsive to glucocorticoids and insulin and also regulates HPA axis responsivity at a site proximal to CRF neurons. Ann NY Acad Sci, 1995,771:730.
    [41] Emilsson V et al.Expression of the functional Leptin receptor mRNA in pancreatic islets and direct inhibitory action of Leptin on insulin secretion.Diabetes,1997, 46:313 一 316.
    [42] Vos PD, Lefebvre AM, Shrivo I, et al.Glucocorticoids induce the expression of the Leptin gene through a nonclassical mechanism of transcriptional activation. J Biol Chem,1998, 273:619-626.
    [43] Banks WA, Kastin AJ, Huang W, et al.Leptin enters the brain by a saturable system independent of insulin. Peptides, 1996,17:305-311
    [44] Mounzih K, Lu R, and Chehab F F. Leptin treatment rescues the sterility of genetically obese ob/ob males. Endocrinology.1997. 138:1190-1193.
    [45] Cheung CC, Thornton JE, Kuijeer JL, et al.Leptin is a metabolic gate for the onset of puberty in the female rat. Endocrinology,1997,138(2):855-858.
    [46] Mercer JG, Hoggard N, Williams L et al.Coexpression of Leptin receptor and preproneuropeptide Y mRNA in arcute nucleus of mouse hypothalamus.J Neuroendocrinol,1996, 8:733-735.
    [47] Lord GM, Matarese G, Howard JK, et al. Leptin modulates the T-cell immune response and reverses starvation 一 induced immunosuppression. Nature,1998, 394:897 一 901.
    [48] Loffreda S, Yang SQ,Lin HZ, et al.Leptin regulates proinflammatory immune responses. The FASEB Journal.1998. 12:57-65.
    [49] Cao RH, Brakenhielm E, Wahlestedt C, et al.Leptin induces vascular permeability and synergistically stimulates angiogenesis with FGF-2 and VEGF. Proc Natl Acad Sci USA,2001,98:6390-6395
    [50] Gasow A, Haidan A, Hilbers U. et al.Expression of Leptin receptor in normal human adrenals differential regulation of adrenocortical and adrenomedullary function by letpin.Journal of Clinical Endocrinol Metab, 1998, 84:4459-4466.
    [51] Kain ZN, et al.Leptin and perioperative neuroendocrinological stress response. Journal of Clinical Endocrinol Metab, 1999,84:2438 一 2442.
    [52] Marikovsky M, Rosenblum CI, Faltin Z, et al.Appearance of Leptin in wound fluid as a response to injury. Wound Repair Regen. 2002 Sep-Oct, 10 (5):302-307.
    [53] Ahima RS, Prabakaran D, Mantzoros C, et al.Role of Leptin in the neuroendocrine response to fasting. Nature, 1996, 382:250-252.
    [54] Chen XL, Dean R G, Hausman G J. Expression of Leptin mRNA and CCAAT-enhancer binding proteins in response to insulin deprivation during preadipocyte differentiation in primary cultures of porcine stromalvascular cells. Dourest Anim Endocrino1, 1999,17: 389-401.
    [55] Chen G, Koyama K, Yuan X, et al. Disappearance of body fat in normal rats induced by adenovirus-mediated Leptin gene therapy. Proc Natl Acad Sci USA. 1996, 93:14795-14799.
    [56] Kennes YM, Murphy BD, Pothier F, et al.Characterization of swine Leptin(Lep) polymorphisms and their association with production traits, Animal Genetics,2001,32:215-218.
    [57] Cameron ND, Penman JC, McCullough E. Serum Leptin concentration in pigs selected for high or low daily food intake. Genet Res,2000,75 (2):209-213.
    [58] Geary TW, McFadin EL, MacNeil MD, et al.Leptin as a predictor of carcass composition in beef cattle. J Anim Sci, 2003 81:1-8.
    [59] Clancy M, HannahLC. Splicing of the maize Sh1 first intron is essential for enhancement of gene expression, and a T-richmotif increases expression without affecting splicing[J].Plant Physiol, 2002,130(2): 918-929.
    [60] Bachl J, Olsson C, Chitkara N,et al. The Igmutator is dependent on the presence, position and orientation of the large intron enhancer[J].Proc Natl Acad Sci USA, 1998, 95(5): 2396-2399.
    [61] Chen J, HayesP, RoyK,et al. Two promoters regulate transcription of the mouse folylpolyglutamate synthetase gene three tightly clustered Spl sites within the first intron markedly enhance activity ofpromoter B[J].Gene, 2000,242(1-2):257-264.
    [62] Surinya KH, CoxTC, May BK.et al. Identification and characterization of a conserved erythroid-specific enhancer located in intron 8 of the human 5-aminolevulinate synthase 2 gene[J].J Biol Chem.,1998, 273(27): 16798-16809.
    [63] Palmiter RD, Sandgren EP, Avarbock MR,et al. Heterologouse introns can enhence expression of transgenes in mice[J].Proc Natl Acad Sci USA,1991, 88(2):478-482.
    [64] Luehrsen KR, Walbot V. Intron enhancement of gene expression and the splicing efficiency of introns in maize cells[J].Mol Gen Genet, 1991, 225(1): 81-93.
    [65] Nott A, Meislin SH, MooreMJ. Aquantitative analysisof intron effectson mammalian gene expression[J].RNA, 2003, 9(5): 607-617.
    [66] ManiatisT, Reed R. An extensive network of coupling amonggene expres-sion machines[J].Nature, 2002,416 (6880):499-506.
    [67] Furger A, O’Sullivan JM, Binnie A,et al. Promoter proximal splice sites enhance transcription[J].Genes Dev., 2002,16(21):2792-2799.
    [68] Manley JL. Nuclear coupling: RNA processing reaches back to transcrip-tion[J].Nat Struct Biol., 2002, 9(11):790-791.
    [69] Hamer DH, Leder P. Splicing and the formation of stable RNA[J].Cell,1979,18 (4): 1299-1302.
    [70] Lu S, Cullen BR. Analysis of the stimulatory effect of splicing on mRNA production and utilization in mammalian cells [J].RNA, 2003, 9(5): 618-630.
    [71] Schaal TD, ManiatisT. Multiple distinct splicing enhancers in the protein-coding sequences of a constitutively spliced pre-mRNA [J].Mol Cell Biol, 1999,19(1):261-273.
    [72] Caudevilla C, Codony C, Serra D,et al. Localization of an exonic splicing enhencer responsible for mammalian natural trans-splicing[J].Nucleic Acids Res, 2001, 29(14): 3108-3115.
    [73] Storbeck CJ, Sabourin LA, Waring JD,et al. Definition of regulatory sequence elements in the promoter region and the first intron of the myotonic dystrophy protein kinase gene [J].J Biol Chem, 1998, 273(15): 9193-9147.
    [74] Lopez AJ. Alternative splicing of pre-mRNA: developmental consequences and mechanisms of regulation [J].Annu Rev Genet, 1998,32:279-305.
    [75] Kriventseva EV, Koch I, Apweiler R, et al. Increase of functional diversity by alternative splicing [J].Trends Genet, 2003, 19(3): 124-128.
    [76] Modrek B, Lee C. Agenomic viewof alternative splicing [J].Nat Genet, 2002, 30(1):13-19.
    [77] Berge SM. Exon recognition in vertebrate splicing [J].J Biol Chem, 1995, 270:2411-2414.
    [78] Graveley BR. Alternative splicing: increasing diversity in the proteomic world [J].Trends Genet, 2001,17 (2): 100-107.
    [79] Choi T, HuangM, Gorman C,et al. Agenetic intron increases gene expression in transgenic mice [J].Mol Cell Biol, 1991,11(6): 3070-3074.
    [80] Svaren J, Chalkley R. The structure and assembly of active chromatin [J].Trends Genet, 1990, 6(2): 52-56.
    [81] Meade H, Gates L, Lacy E,et al. Bovine alpha S1-casein gene sequences direct high level expression of active human urokinase in mouse milk [J].Biotechnology, 1990,8(5): 443-446
    [82] Buitmap J.A microsatellite (BOTO24) located between the bovine IL4and IL13 is polymorphic in cattle and goat [J].Animal-Genetics,1996,27:3,212-213.
    [83] Senese C,A microsatellite Sequence showing polymorphism in sheep,goat,cattle and waterbuffalo[J].Animal-Genetics,1998,29(1):63-72.
    [84] Ganai N.Genetic variation within and among three Indian breeds of goat using heterologous microsatellite markes [J].Animal-Biotechnology, 2001, 12(2): 121-136.
    [85] Wilsom.The isolation and characterization of microsatallite loci bison,and their usefulness in other artiodactyis[J].Animal-Genetics,1999.30 (3),226-227.
    [86] Farid A.Genetic analysia of ten sheep breeds using microsatallite marhers [J].Canadian-Journal-of Animal-Science, 2000, 80(1):9-17.
    [87] Nijman,Thirteen bovine micrisatellite markers that are polymorphic in sheep[J].Animal-Genetic,1998,29(6):474-475
    [88] Stahlberger .Genetic relationships in Swiss breeds based on microsatallite analysis [J].Journal-of-Breedings-and-Genetics, 2001, 118(6):379-387.
    [89] Roed-KH.Microsatellite variation in Scadinavian Cervidae using Primers drived from Bovidae [J].Hereditas-Landskrona,1998, 129:1,19~25.
    [90] 黄银花,李宁,孙汗,等.应用微卫星标记在家畜中定位数量性状主基因[J].第七次全国畜禽遗传标记研讨会论文集,中国南昌,2000,7(1):42-46.
    [91] 张艳,张树义.微卫星方法简介[J].动物学杂志,1999,34(2):42-44.
    [92] 张丽娟,张保军,耿社民.微卫星标记与动物育种[J].黄牛杂志,2003,29(2):49-52.
    [93] 邓学梅.用于鸡基因定位的资源群体的建立和黑色素等质量性状的遗传分析[D].中国农业大学博士论文,2001
    [94] 戚豫,唐炬,黄丽英.DNA 单链构象多态性原理初探[J].基础医学与临床,1997,17(2):142-146.
    [95] 单雪松.奶牛 weaver 基因及其连锁微卫星位点结构、特性和应用的研究[D].中国农业大学博士学位论文,2000.
    [96] 李国华.奶牛乳房炎性状候选基因的分析[D].中国农业大学博士学位论文,2001
    [97] Kenzo Takahashi, Rudolph D.et al.Coulomb Cloning and characterization of multiple human genes and cDNAs sencoding highly related type keratin6 isoform [J]. Biol. chem. 1995,270 (31):18581-18592.
    [98] Kuczek ES, Rogers G E.Sheep wool(glycine+tyrosine)-richkeratin genes.A family of low sequence homology[J].Eur J Biochem.,1987 Jul 1:166(1):79-85.
    [99] Michael A.Rogers.et al.Characterization of aFirst Domain of Human High Glycine-Tyrosine and High Sulfur Keratin-associated Protein (KAP)Gene on Chomosome 2122.1 [J]. Biol. Chem.2002, 277: 48993-49002.
    [100] Michael.A.Rogers.et al.Sheep keratinsLCharacterization of cDNA clones for the glycine+tyrosine-rich wool protein using a synthetic probe Eur [J]. Biochem, 1985,Jan2,146 (1):89-93.
    [101] Betteridge,k, et al.Proceedings of the second international cashmere conference [J]. Lincoin college,New Zealand,1987,137-143.
    [102] Daniel, V., Laurent,S.,et al.A Genetic Linkage Map of the Male Goat Genome [J]. Genetics,1996,144:279-305.
    [103] Dicks P.,et al.The effect of melatonin implants given under different daylength regimes on plasma prolactin concentrations and fibre growth and shedding in cashmere goats [J]. Animal Science,1995,69:239-247.
    [104] Gerstmayr, Sand Horst, P. Estimates of performance traits in Turkish Angora goats [J]. Small Rumin.Res,1995 ,16(2):141-157.
    [105] Henderson, M.et,al.Seasonal variation in the mitotin activity of secondary fiber follicles in adultcashmere goats.Small ruminant research.1992,(6):329-345.
    [106] 张胜利,张沅.标记辅助遗传评定效果的研究[J].北京奶业,1998(2):10-12.
    [107] Zhang.W and Smith.C.Computer simulation of marker assisted selection utilizing linkage disequilibrium, TAG,1992(83):813-820.
    [108] 郭源梅,陈克飞,黄路生,等.标记辅助选择的研究进展[A].第 7 次全国畜禽遗传标记研讨会论文集[C],南昌,2000,64-70.
    [109] 姜长鉴,顾兴友.遗传标记与数量性状间连锁关系的分析[J].遗传,1996,18(2):21-24.
    [110] 蒋思文,彭健.猪育种中 MAS 的分子标记和 QTL[A].第 6 次全国畜禽遗传标记研讨会论文集[C],常州,1998:44-46.
    [111] 马月辉,吴常信,张沅.标记辅助选择及其应用[A].第 6 次全国畜禽遗传标记研讨会论文集[C],常州,1998:16-20.
    [112] 晏兆莉,张成忠.家畜育种中的 MAS 的遗传标记和 QTL[J].西南民族学院学报(自然科学版)1996,22(2):206-210.
    [113] Mcdonal, B .J.,et al.Cyclical fleece growth in cashmere goats[J].Aust J. Aagric. Res., 1987,38: 597-609.
    [114] Restall,B, J.,Pattie.W.A..The inheritance of cashmere in Australian goats[J].Genetic parameters and breeding values,1989,21(3):251-261.
    [115] Rhind,S. M.&S.R.Memillen.Effects of methythiouracil treatment on the growth and moult of cashmere fibre in goats[J].Animal Science,1996,62(3):513-520.
    [116] Zhou.Huanmin,D.Allain,Li.Jinquan et al.Effects of non-genetic factors on production traits of Inner Mongolia cashmere goats in China,2001
    [117] 祁玉香,余忠祥.欧拉型藏羊[J].中国草食动物.2006.26.4:61~63
    [118] 刘永峰,王金越. Leptin 的生物学特征及其在控体重方面机制的研究[J].广州体育学院学报.2006.26.3:95~98
    [119] Ahima.R.S et al Role of leptin in the neuroendocrine response to fasting [J]. Nature 1996, 382, 250-252
    [120] 毕晋明,王永军.动物脂肪性状相关基因的效应调控研究进展[J],中国畜牧兽医,2006.33.7:49~51
    [121] 张亚妮,张恩平,等. KAP 基因的多态性与辽宁绒山羊经济性状的关系研究[J].中国农业科学.2007.40(9):2062~2067
    [122] 盛志廉,陈瑶生.数量遗传学.北京:科学出版社,1999

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