首页> 外文期刊>Photochemistry and Photobiology: An International Journal >NONMAMMALIAN MODELS FOR SUNLIGHT CARCINOGENESIS - GENETIC ANALYSIS OF MELANOMA FORMATION IN XIPHOPHORUS HYBRID FISH
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NONMAMMALIAN MODELS FOR SUNLIGHT CARCINOGENESIS - GENETIC ANALYSIS OF MELANOMA FORMATION IN XIPHOPHORUS HYBRID FISH

机译:日光致癌的非哺乳动物模型-鳞翅目杂交鱼黑色素形成的遗传分析

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Genetic hybrids of Xiphophorus fishes have been used for decades to study heritable melanoma formation. In these models, overexpression of pigmentation patterns from melanin-producing pigment cells can lead to genetically regulated melanoma formation in backcross hybrids, In the best studied of these models, the Gordon-Kosswig hybrid melanoma, tumors form spontaneously in all individuals of a subset of backcross hybrids between the platyfish Xiphophorus maculatus Jp 163 A and the swordtail species Xiphophorus helleri. Backcross hybrids susceptible to melanoma formation inherit a sea-linked oncogene, Xmrk, associated with the spotted dorsal (Sd) pigment pattern and have lost both copies of an autosomal gene, DIFF, from the X. maculatus parent, Spontaneous melanoma formation conforms to simple, two-gene Mendelian inheritance in which DIFF behaves as a recessive tumor suppressor gene, Recently, Xiphophorus hybrids in which melanomas can be induced by UV and near-UV visible light exposure have been described, We report here results of genetic linkage analysis of one of these Xiphophorus light-inducible hybrid melanoma models, in backcross hybrids between the two platyfish species X, maculatus Jp 163 B and Xiphophorus; couchianus. Our linkage results provide the first estimate of recombination between the tumor suppressor locus, DIFF, and glycerate-2-dehydrogenase (GLYDH) in Xiphophorus linkage group V. Also, they demonstrate that DIFF regulates hyperplasia of spotted side (Sp) pigment cells in this hybrid model, analogous to its regulation of hyperplasia of Sd pigment cells in the ''classical'' Gordon-Kosswig hybrid. Joint segregation analyses of melanoma-bearing fish indicate that segregation of DIFF is genetically linked to melanoma induction by 405 nm light in this model but that induction of melanomas by UV wavelengths apparently does not depend on segregation of the DIFF locus. [References: 53]
机译:Xiphophorus鱼的遗传杂种已经被用于研究遗传性黑色素瘤的形成数十年。在这些模型中,产生黑色素的色素细胞中色素沉着模式的过度表达可导致回交杂种中遗传调控的黑色素瘤的形成。在这些模型的最佳研究中,戈登-科斯维格杂交黑色素瘤在所有亚型的个体中均自发形成。斑鱼Xiphophorus maculatus Jp 163 A和剑尾物种Xiphophorus helleri之间的回交杂种。易受黑色素瘤形成影响的回交杂种继承了与斑点背(Sd)色素斑纹相关的海联癌基因Xmrk,并失去了来自X. maculatus亲本的常染色体基因DIFF的两个拷贝,自发黑色素瘤形成符合简单,其中DIFF表现为隐性肿瘤抑制基因的两基因孟德尔遗传,最近,已经描述了Xiphophorus杂种,其中紫外线和近紫外可见光可以诱导黑色素瘤,我们在此报告其中一种的遗传连锁分析结果这些Xiphophorus光诱导的杂交黑素瘤模型中的两个,在两个鳞甲类鱼类X,黄斑鱼Jp 163 B和Xiphophorus之间的回交杂种中;沙发。我们的连锁结果首次估计了Xiphophorus连锁组V中抑癌基因座,DIFF和甘油2-脱氢酶(GLYDH)的重组。此外,他们还证明DIFF可以调节斑点侧(Sp)色素细胞的增生。杂交模型,类似于其对“经典”戈登-科斯维格杂交种中Sd色素细胞增生的调控。含黑素瘤鱼的联合分离分析表明,在此模型中,DIFF的分离与405 nm光诱导的黑素瘤遗传相关,但UV波长诱导的黑素瘤显然并不取决于DIFF基因座的分离。 [参考:53]

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