Properties of T antigens induced by wild-type SV40 and tsA mutants in lytic infection
Properties of T antigens induced by wild-type SV40 and tsA mutants in lytic infection
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野生型 SV40 和 tsA 突变体在裂解感染中诱导的 T 抗原的特性
DOI：
10.1016/0092-8674(75)90042-2
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发表时间：
1975
期刊：
影响因子：
64.5
通讯作者：
G. Stark
中科院分区：
文献类型：
--
作者：
J. Alwine;S. Reed;J. Ferguson;G. Stark
通过补体结合测定，感染tsA突变体的细胞提取物中的T抗原在32 ℃或41 ℃下的不稳定性是感染野生型SV 40的细胞提取物中的抗原的2至6倍。野生型和突变型抗原的稳定性不因混合提取物而改变，因此稳定性是每种抗原的固有性质，不受提取物的另一组分的影响。这一观察结果表明，T抗原可能是A基因的病毒编码产物。在32 ℃的容许温度下用高多样性的野生型或tsA突变病毒感染的细胞中，T抗原的量大致相等，并且在整个感染期间（最多96小时）呈递增趋势。在32 ℃下用野生型和tsA病毒的混合物感染96小时的细胞产生具有野生型稳定性的T抗原，即使当用高达5倍过量的突变体进行感染时。更稳定的野生型抗原可以直接或间接抑制更不稳定的突变型抗原的合成。T抗原是在被猿猴病毒40（SV40）感染或转化的细胞中检测到的特征性蛋白质。虽然其功能和起源尚未确定，但最近的观察表明T抗原参与病毒DNA复制的起始，并且可能是SV 40 A基因的产物。Tegtmeyer（1972）发现A互补组的温度敏感突变体（tsA突变体）不能在非允许温度下启动病毒DNA复制，Robb et al.（1974）报道了tsA突变体在非允许温度下不诱导正常水平的T抗原。与在DNA复制中的可能作用相关，T抗原优先在复制起点处或附近与SV40 DNA结合（Reed等人，1975年）。在本文中，我们提出的数据表明，在tsA突变体的缺陷是在T抗原的结构基因。我们还发现了与T抗原调节自身合成的假设一致的证据（Tegtmeyer，1974）。
T antigen in extracts of cells infected with tsA mutants is 2 to 6 times more labile at 32 C or 41 C than the antigen in extracts of cells infected with wild-type SV40, as assayed by complement fixation. The stabilities of wild-type and mutant antigens are not altered by mixing the extracts, and thus the stability is an intrinsic property of each antigen and is not determined by another component of the extract. This observation indicates that T antigen is probably the virus-coded product of the A gene. in cells infected at the permissive temperature of 32 C with a high multiplicity of either wild-type or tsA mutant virus, the amounts of T antigen are approximately equivalent and increase logarithmically during the entire period of infection, up to 96 hr. Cells infected at 32 C for 96 hr with mixtures of wild-type and tsA virus produce T antigen with the stability of wild-type, even when the infection is carried out with up to a 5 fold excess of the mutant. The more stable wild-type antigen may repress, directly or indirectly, the synthesis of the more labile mutant antigen.T antigen is a protein characteristically detected in cells infected or transformed by Simian Virus 40 (SV40). Although its function and origin have not yet been defined, recent observations indicate that T antigen is involved in the initiation of viral DNA replication and may be the product of the SV40 A gene. Tegtmeyer(1972) found that temperature-sensitive mutants of the A complementation group (tsA mutants) are unable to initiate viral DNA replication at nonpermissive temperatures, and Robb et al.(1974) reported that tsA mutants do not induce normal levels of T antigen at a nonpermissive temperature. Relevant to a possible role in DNA replication, T antigen binds to SV40 DNA preferentially at or near the origin of replication(Reed et al., 1975). In this paper, we present data which suggest that the defect in tsA mutants is in the structural gene for T antigen. We have also found evidence consistent with the hypothesis that T antigen regulates its own synthesis (Tegtmeyer, 1974).