ANIMAL MODEL OF GLOBOID CELL LEUKODYSTROPHY IN RHESUS MONKEYS

为了研究伯氏疏螺旋体蛋白在 其表达响应于培养温度、菌株 Sh-2-82螺旋体体外连续传代16次。 在连续传代后，对该菌株的蛋白质和质粒DNA谱进行了分析。 将第16代变异体与低传代（第16代）变异体进行比较， 3)亲本培养以评估蛋白质表达的损失， 质粒DNA。 亲本培养物中16种抗原的表达 在较高的孵育温度下， 体温34？C，而不是在24？C. 一 16种亲本抗原中的大多数随后在 更高的传代变异。 这些抗原表达的缺失， 更高的传代变异也与 对C3 H/HeN小鼠的感染性。 16种抗原中有两种是 被鉴定为脂蛋白OspC，这是一种以前已知的 温度诱导（史蒂文森，B. T. G. Schwan和P.A.罗莎 Infect. Immun. 63：4535-4539，1995）和P35。 抗原的丢失 然而，表达不能与可检测到的 质粒序列;具体地，携带ospC和 发现P35基因均保留在第16代变体中。 OspC和P35在亲本中的温度诱导表达 SH-2-82螺旋体及其在大肠杆菌中的最低表达水平 第16代变异体，两者均与 对应的mRNA。 这些数据表明 温度诱导抗原对于感染性是必需的， 这些抗原中至少两种OspC和 P35在转录水平上受到控制。 供资基础 出版物

In an effort to study the role of Borrelia burgdorferi proteins whose expression respond to changes in culture temperature, strain Sh-2-82 spirochetes were serially passaged 16 times in vitro. Following serial passage, the protein and plasmid DNA profiles of the passage 16 variant were compared with that of the low-passage (passage 3) parental culture to assess the loss of protein expression and plasmid DNAs. The expression of 16 antigens in the parental culture was found to be selectively induced at the higher incubation temperature of 34?C and not at the lower temperature of 24?C. A majority of the 16 parental antigens were subsequently lost in the higher passage variant. The loss of expression of these antigens in the higher passage variant also correlated with the loss of infectivity for the C3H/HeN mouse. Two of the 16 antigens were identified as the lipoproteins OspC, an antigen previously known to be temperature-inducible (Stevenson, B. T. G. Schwan, and P. A. Rosa, Infect. Immun. 63:4535-4539, 1995) and P35. The loss of antigen expression could not be correlated, however, with a detectable loss of plasmid sequences; specifically, the plasmids carrying the ospC and P35 genes were both found to be retained in the passage 16 variant. The temperature-inducible expression of OspC and P35 in the parental Sh-2-82 spirochetes and their minimal levels of expression in the passage 16 variant, both correlated with the steady state levels of the corresponding mRNAs. These data suggest that temperature-inducible antigens are essential for infectivity and that the regulated expression of at least two of these antigens, OspC and P35, is controlled at the transcriptional level. FUNDING Base PUBLICATIONS None