FINE-STRUCTURE PHYSICAL MAP LOCATIONS OF ALTERATIONS THAT AFFECT CELL-FUSION IN HERPES-SIMPLEX VIRUS TYPE-1

FINE-STRUCTURE PHYSICAL MAP LOCATIONS OF ALTERATIONS THAT AFFECT CELL-FUSION IN HERPES-SIMPLEX VIRUS TYPE-1
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DOI:
10.1016/0042-6822(84)90042-4
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发表时间:
1984-01-01
期刊:
影响因子:
3.7
通讯作者:
PERSON, S
PERSON, S
中科院分区:
医学3区
文献类型:
--
作者:
BOND, VC;PERSON, S

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测定了1型单纯疱疹病毒(HSV-1)合胞突变体MP、syn-20、syn-102、syn-103和syn-105的精细结构物理图谱位置。除MP外,其余均来自KOS菌株。MP包含多种突变,包括导致糖蛋白gC积累丧失的突变。在原型图谱坐标0.707-0810范围内构建重叠的DNA亚克隆。这些与完整的突变DNA一起用于拯救syn标记。所有突变体的突变均通过KOS DNA序列在0.732 ~ 0.745之间获救。这种依赖细胞的同步突变是kos衍生突变体中唯一的病变。MP的第二个syn突变被定位在坐标0.745-0.753。这种病变产生较少的融合,也依赖于融合表型的细胞类型。独立于细胞类型的融合需要两种突变的存在。用间接免疫荧光法测定了菌株MP中糖蛋白C (gC)产生的位点,座标为0.745-0.753。ICP-27的核苷酸序列,即刻早期或。α。功能未知的蛋白质,在这些坐标内。由于gC的产生和syn表型可以通过重组分离,它们一定是由独立的突变引起的。
Fine structure physical map locations were determined for syncytial mutants (MP, syn-20, syn-102, syn-103 and syn-105) of herpes simplex virus type 1 (HSV-1). All except MP were derived from the KOS strain. MP contains multiple mutations, including one that leads to the loss of accumulation of glycoprotein gC. Overlapping DNA subclones within the prototypic map coordinates 0.707-0810 were constructed from a library of KOS fragments. These were used along with intact mutant DNA to rescue the syn marker. Mutations in all of the mutants were rescued by KOS DNA sequences between 0.732 and 0.745. This cell-dependent syn mutation is the only lesion in the KOS-derived mutants. A second syn mutation in MP was mapped at coordinates 0.745-0.753. This lesion produces less fusion and is also cell-type dependent for the fusion phenotype. Cell-type independent fusion requires the presence of both mutations. The locus determining glycoprotein C (gC) production in strain MP was also mapped, using indirect immunofluorescence, to coordinates 0.745-0.753. Nucleotide sequences for ICP-27, an immediate early or .alpha. protein of unknown function, are within these coordinates. Since gC production and the syn phenotype are separable by recombination, they must be caused by independent mutations.