Efficiency Alleles of the Pctr1 Modifier Locus for Plasmacytoma Susceptibility

Shuling-L. Zhang; Wendy DuBois; Edward S. Ramsay; Valeri Bliskovski; Herbert C. Morse; Leki Taddesse-Heath; William C. Vass; Ronald A. DePinho; Beverly A. Mock

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Efficiency Alleles of the Pctr1 Modifier Locus for Plasmacytoma Susceptibility

机译：Pctr1修饰位点对浆细胞瘤易感性的效率等位基因

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The susceptibility of BALB/c mice to pristane-induced plasmacytomas is a complex genetic trait involving multiple loci, while DBA/2 and C57BL/6 strains are genetically resistant to the plasmacytomagenic effects of pristane. In this model system for human B-cell neoplasia, one of the BALB/c susceptibility and modifier loci, Pctr1, was mapped to a 5.7-centimorgan (cM) chromosomal region that includedCdkn2a, which encodes p16INK4a and p19ARF, and the coding sequences for the BALB/c p16INK4a and p19ARF alleles were found to be polymorphic with respect to their resistant Pctr1counterparts in DBA/2 and C57BL/6 mice (45). In the present study, alleles of Pctr1, Cdkn2a, andD4Mit15 from a resistant strain (BALB/cDAG) carrying DBA/2 chromatin were introgressively backcrossed to the susceptible BALB/c strain. The resultant C.DAG-Pctr1 Cdkn2a D4Mit15 congenic was more resistant to plasmacytomagenesis than BALB/c, thus narrowingPctr1 to a 1.5-cM interval. Concomitantly, resistant C57BL/6 mice, from which both gene products of the Cdkn2agene have been eliminated, developed pristane-induced plasma cell tumors over a shorter latency period than the traditionally susceptible BALB/cAn strain. Biological assays of the p16INK4a and p19ARF alleles from BALB/c and DBA/2 indicated that the BALB/c p16INK4a allele was less active than its DBA/2 counterpart in inducing growth arrest of mouse plasmacytoma cell lines and preventing ras-induced transformation of NIH 3T3 cells, while the two p19ARF alleles displayed similar potencies in both assays. We propose that the BALB/c susceptibility/modifier locus,Pctr1, is an “efficiency” allele of the p16INK4a gene.

机译：BALB / c小鼠对p烷诱导的浆细胞瘤的敏感性是一个复杂的遗传特征，涉及多个基因座，而DBA / 2和C57BL / 6株对rist烷的浆细胞瘤作用具有遗传抗性。在此用于人类B细胞瘤形成的模型系统中，将BALB / c易感性和修饰位点之一 Pctr1 映射到一个5.7 centimorgan（cM）染色体区域，该区域包括 Cdkn2a < / em>，它编码p16 INK4a 和p19 ARF ，以及BALB / c p16 INK4a 和p19 ARF的编码序列等位基因在其对DBA / 2和C57BL / 6小鼠的抗性 Pctr1 对应物中具有多态性（45）。在本研究中，来自携带DBA / 2染色质的抗性菌株（BALB / cDAG）的 Pctr1 ， Cdkn2a 和 D4Mit15 等位基因是渐渗的与易感的BALB / c菌株回交。所得的C.DAG- Pctr1 Cdkn2a D4Mit15 同系物比BALB / c更耐浆细胞生成，因此将 Pctr1 范围缩小到1.5-cM。同时，从中消除了 Cdkn2a 基因的两个基因产物的抗性C57BL / 6小鼠，比传统上易感的BALB / cAn株在更短的潜伏期内发展出了rist烷诱导的浆细胞肿瘤。对来自BALB / c和DBA / 2的p16 INK4a 和p19 ARF 等位基因的生物学分析表明，BALB / c p16 INK4a 等位基因较少比DBA / 2具有更高的活性，可诱导小鼠浆细胞瘤细胞系生长停滞并阻止 ras 诱导的NIH 3T3细胞转化，而两个p19 ARF 等位基因显示出相似的效价在两种测定中。我们认为，BALB / c易感性/修饰位点 Pctr1 是p16 INK4a 基因的“有效”等位基因。 展开▼

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《Molecular and Cellular Biology》 |2001年第1期|共9页

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Shuling-L. Zhang; Wendy DuBois; Edward S. Ramsay; Valeri Bliskovski; Herbert C. Morse; Leki Taddesse-Heath; William C. Vass; Ronald A. DePinho; Beverly A. Mock;
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中图分类细胞生物学;

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Efficiency Alleles of the Pctr1 Modifier Locus for Plasmacytoma Susceptibility

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