马毛色遗传机理研究进展

动物毛色是人类正向选择产生的表型之一,在遗传与进化过程中扮演着重要角色。其中马的毛色丰富多变,单从表型无法准确判别其属于哪种毛色,造成马品种登记时毛色性状记录不准确,因此研究马毛色形成机理在育种工作中具有重要意义。随着基因组学及测序技术的日益成熟,马毛色形成遗传机理的研究不断深入,并发现不同毛色性状与特定疾病之间的相关性。本文从遗传学的角度对马的毛色进行归类,对与其形成的相关基因、作用机理及应用等研究进展进行了综述,以期为马毛色形成机理的系统性研究和马匹选育提供借鉴和参考。     

马匹毛色遗传规律的调查

毛色不仅是品种的特征,也与马的气质、用途息息相关,所以在育种和交易中,人们对毛色总有不同的嗜好,购买役畜时,早就有“青马狸牛”之说。伊犁马是我国的名马,为进步提高其品质,采用奥尔咯夫菊花青公马进行杂交改良,但后代毛色分离很大。为探求毛色遗传的规律和衡量人们对毛色分类的叫法与遗传的联系,我们对5匹马纯种菊花青公马与102母匹马交配产驹结果,进行了调查与分析、其结果归综如下:一、资料统计与计算     

白化黑线仓鼠的毛色遗传

毛色遗传分析证实，红眼白色仓鼠和野生色仓鼠交配的Ｆ１杂合子呈野生色，在Ｆ２（子二代）中野生色与白色分离比率为３∶１，回交（ＢＣ）子代中（白×Ｆ１）野生色与白色的比例是１∶１。结果表明黑线仓鼠白化性状属单一隐性遗传，由常染色体上一个隐性基因控制。     

虎毛色多样性的遗传演化

虎是世界上最大的猫科动物,也是豹属(虎、狮、豹、美洲豹、雪豹)中唯一具条纹而不是斑点的物种。虎以黄底黑纹的野生型标志性毛皮为世人所熟知,此外,有白虎、金虎、雪虎、黑虎等具毛色多态型,其遗传起源及科学和保育价值则长期存在疑问和争议。最近10年基因组学技术的发展,定位了Slc45a2、Corin、Taqpep等参与和调控色素通路并导致虎毛色变异的基因,揭示了其对物种生存和适应的潜在影响。虎毛色多样性遗传机制的揭示,为虎的保护及圈养繁殖提供了科学佐证,也为通过非模式生物研究动物适应性演化进行了积极探索。     

白色基因座(I)在中国地方猪种毛色遗传中的作用研究

通过利用PCR—RFLP和PCR—SSCP技术对中国地方猪种KIT基因内含子17、18的序列进行多态性分析。结果表明：内含子17上的替换突变(G→A)发生于毛色为白色的个体——白色五指山猪、大白猪、长白猪上,其基因型(AB型)频率分别为1、1和0．8;其他中国地方猪种的此基因型频率均为0。内含子18上的缺失突变(AGTT)也同样发生在上述3个猪种的白色个体中,其基因型(AA型)频率分别为1、1和0．93;而且同样在其他的地方品种中其基因型频率均为0。这充分证明KIT基因对于猪的白毛色有重要的调控作用,而且I基因座对于其他的经典遗传基因座有上位作用。另一方面,中国地方猪种荣昌猪虽然在表型上与引入猪种大白猪、长白猪相似(白毛色),但是在KIT基因上发生的突变完全不同,推测它们分别属于不同的毛色遗传体系。     

滩羊裘皮毛色调控基因的研究进展

滩羊是中国裘皮来源的珍稀地方绵羊品种,以所产二毛裘皮而著称,二毛裘皮在国内外毛皮市场上均享有较高的声誉。毛色是宁夏滩羊重要的经济性状,滩羊多为体躯白色,头部有黑褐斑,个别个体黑头或体躯黑杂色,少数纯白。毛色与体内黑色素的数量、种类和分布等情况有关。掌握调控滩羊毛色基因的作用机制,可以有效控制其毛色性状。本文从滩羊的裘皮特性、毛色形成机理、毛色相关基因(MC1R基因、Agouti基因、TYR基因、MITF基因和KIT基因)的功能及选择信号检测等方面进行了综述。     

小鼠毛色遗传的控制机制及其在遗传学教学中的应用

小鼠是最常用的哺乳动物模式生物,其毛色有白色、灰色、黄色、黑色等,是典型的孟德尔遗传性状。但在本科遗传学教学中,一般只在介绍隐性致死基因的时候才提到小鼠毛色遗传的例子。作者深入挖掘和整理了小鼠毛色遗传的分子机制,并把这个例子贯穿于讲解孟德尔遗传以及介绍分子遗传学的基因结构、基因功能、基因调控、基因互作、基因的表观遗传学修饰和数量性状遗传等,尝试用同一个案例贯穿本科遗传学教学,培养学生建立由表及里的系统分析能力,既凸显遗传学研究的前沿性和完整性,又吸引了学生的注意力,激发了学生的学习兴趣,收到了很好的教学效果。     

MC1R基因多态性与豚鼠隐性黄毛色的相关性分析

豚鼠Cavia porcellus的隐性黄毛色表型是由编码黑素皮质激素受体1(MC1R)的extension基因座位的等位基因e控制。本研究对野生型和黄毛色豚鼠MC1R基因位点所在区域进行PCR扩增与测序发现,在黄毛色豚鼠中存在1个2 760 bp的基因组缺失,该缺失涵盖了MC1R基因的整个编码区。采用三引物扩增体系对豚鼠MC1R基因缺失突变进行群体基因分型,在随机选择的58只野生型个体中,36只为EE纯合子,22只为Ee杂合子,而31只黄毛色个体均为ee纯合子;在15只测交后代中,8只黄毛色个体均为ee纯合子,而7只野生型个体均为Ee杂合子。基因分型结果表明,MC1R基因2 760 bp的缺失与隐性黄毛色完全相关。本研究为进一步探究MC1R基因在哺乳动物毛色遗传机制中的作用以及豚鼠的分子标记辅助育种提供了理论依据。     

猪黑素皮质素受体1(MC1R)基因与毛色表型的研究

猪的毛色表型虽然与经济性状没有直接相关,但它却对经济效益产生重要影响,在猪育种实践、商品猪生产等方面都有应用。结合PCR—AccⅡ—RFIP、PCR—BspH I—RFLP及PCR-SSCP技术,分析了16个全同胞家系和金华猪、嘉兴黑猪、玉山黑猪、乐平花猪、上高两头乌猪及嵊县花猪等6个地方猪种随机采样个体的黑素皮质素受体1(MCIR)基因型。结果显示,地方猪种在MCIR位点携带高频率的显性黑等位基因E^DI,表明我国地方猪种的黑毛色可能主要由显性黑等位基因E^DI调控。通过对嵊县花猪MCIR位点的分析,首次发现PCR-SSCP证据的新序列,与已知的其他5个等位基因带型不同。家系个体的分析结果进一步验证了E^DI对E^p、e为完全显性,E^p对e为不完全显性。     

DXB／c小鼠毛色基因的测试

ＤＸＢ／ｃ小鼠毛色基因的测试牛荣,魏泓,焦有烈,史燕燕,郑亚萍１．重庆第三军医大学实验动物中心重庆６３００３８２．军事医学科学院遗传上的高度纯合性是对近交系动物的基本要求。在于近交系小鼠的遗传监测方法,国际上通用的已有很多。其中,毛色基因的测定是近交...     

The molecular genetics of color vision and color blindness

Recent reports from several laboratories have changed our thinking about the molecular genetics of normal color vision and color blindness. The impact of these new findings can be best appreciated by examining them in the context of the historical development of color vision theory.     

Nomenclature in genetics of sheep color

The International Committee (COGNOSAG) was founded in 1984 with the view of development of nomenclature and analysis of genetic determination of wool and hair colour, visible traits and polymorphisms. At the Workshop 3 of COGNOSAG (July 1988) the completed variant of colour genes' and alleles' list was worked out. The type of phenotypic expression of alleles of genes A, B, C, E, Ph, Rn, S, Sp, SuB and SuS is shown.     

Molecular basis of abnormal red-green color vision: a family with three types of color vision defects

The molecular nature of three different types of X-linked color-vision defects, protanomaly, deuteranomaly, and protanopia, in a large 3-generation family was determined. In the protanomalous and protanopic males the normal red pigment gene was replaced by a 5' red-3' green fusion gene. The protanomalous male had more red pigment DNA in his fusion gene than did the more severely affected protanopic individual. The deuteranomalous individual had four green pigment genes and one 5' green-3' red fusion gene. These results extend those of Nathans et al., who proposed that most red-green color-vision defects arise as a result of unequal crossing-over between the red and green pigment genes. The various data suggest that differences in severity of color-vision defects associated with fusion genes are caused by differences in crossover sites between the red and green pigment genes. Currently used molecular methodology is not sufficiently sensitive to define these fusion points accurately, and the specific color-vision defect within the deutan or protan class cannot be predicted. The DNA patterns for color-vision genes of female heterozygotes have not previously been described. Patterns of heterozygotes may not be distinguishable from those of normals. However, a definite assignment of the various color pigment gene arrays could be carried out by family study. Two compound heterozygotes for color-vision defects who tested as normal by anomaloscopy were found to carry abnormal fusion genes. In addition, a normal red pigment gene was present on one chromosome and at least one normal green pigment gene was present on the other.(ABSTRACT TRUNCATED AT 250 WORDS)     

Molecular basis of the silkworm mutant rel causing red egg color and embryonic death

The coloration and hatchability of insect eggs can affect individual and population survival. However, few genetic loci have been documented to affect both traits, and the genes involved in regulating these two traits are unclear. The silkworm recessive mutant re^l shows both red egg color and embryo mortality. We studied the molecular basis of the re^l phenotype formation. Through genetic analysis, gene screening and sequencing, we found that two closely linked genes, BGIBMGA003497 (Bm-re) and BGIBMGA003697 (BmSema1a), control egg color and embryo mortality, respectively. Six base pairs of the Bm-re gene are deleted in its open reading frame, and BmSema1a is expressed at abnormally low levels in mutant re^l. BmSema1a gene function verification was performed using RNA interference and clustered randomly interspersed palindromic repeats (CRISPR)/CRISPR-associate protein 9. Deficiency of the BmSema1a gene can cause the death of silkworm embryos. This study revealed the molecular basis of silkworm re^l mutant formation and indicated that the Sema1a gene is essential for insect embryo development.