Contreras R, Cole C, Berg P, Fiers W
J Virol. 1979 Feb;29(2):789-93. doi: 10.1128/JVI.29.2.789-793.1979.
Two mutants of simian virus 40, dl-1261 and dl-1262, have deletions that map between coordinated 0.90 and 0.95 (Cole et al., J. Virol 24:277--294, 1977). Both affect the structure of the two minor proteins VP2 and VP3. The precise location and size of the deletions have now been determined by nucleotide sequence analysis. Mutant dl-1261 is deleted of 54 base pairs, is temperature sensitive for the protein defined by the D complementation group, and promotes the synthesis of shorter VP2 and VP3 polypeptides. Mutant dl-1262 is viable irrespective of temperature and has a deletion of 36 base pairs, 23 of which overlap the deletion in dl-1261. Since these mutants produce normal VP1, the deleted regions probably have no function in the splicing of precursor RNA to the VP1 mRNA.
猿猴病毒40的两个突变体dl-1261和dl-1262,其缺失区域定位在坐标0.90至0.95之间(科尔等人,《病毒学杂志》24:277 - 294,1977年)。两者都影响两种次要蛋白质VP2和VP3的结构。现在已通过核苷酸序列分析确定了缺失的精确位置和大小。突变体dl-1261缺失54个碱基对,对由D互补组定义的蛋白质具有温度敏感性,并促进较短的VP2和VP3多肽的合成。突变体dl-1262无论温度如何都能存活,缺失36个碱基对,其中23个与dl-1261中的缺失重叠。由于这些突变体产生正常的VP1,缺失区域可能在前体RNA剪接成VP1 mRNA的过程中没有功能。