Tomilo M, Wilkinson K S, Ryan P
Department of Microbiology and Immunology, University of Tennessee, Memphis 38163.
J Biol Chem. 1994 Dec 16;269(50):32016-21.
We have characterized several mutants that contain alterations in the hydrophilic domain (N region) of the pseudorabies virus glycoprotein gC signal sequence. In general, our results agree with previous findings and indicate that basic residues in the N region are not essential for efficient export of gC in infected cells. While reducing the N region to a net neutral charge led to a slight impairment of membrane translocation, a substantial gC export defect was not observed until a net negative charge was introduced. However, there was one exception to this pattern. The substitution of a leucine for an arginine at the carboxyl terminus of the N region led to a considerable export defect despite maintaining a net positive charge. As a consequence of the substitution, the mutant signal sequence was 1.5 times more hydrophobic than wild type, but we found that the defect could be largely corrected if an additional alteration that lessened the overall hydrophobicity of the gC signal sequence was incorporated. We suggest that an upper limit of hydrophobicity may exist for eukaryotic signal sequences; exceeding this value could lead to an export defect.
我们已经鉴定了几种突变体,这些突变体在伪狂犬病病毒糖蛋白gC信号序列的亲水区(N区)存在改变。总体而言,我们的结果与先前的发现一致,表明N区中的碱性残基对于gC在感染细胞中的有效输出并非必不可少。虽然将N区减少到净中性电荷会导致膜转运略有受损,但直到引入净负电荷才观察到明显的gC输出缺陷。然而,这种模式有一个例外。在N区羧基末端将亮氨酸替换为精氨酸导致了相当大的输出缺陷,尽管保持了净正电荷。作为替换的结果,突变信号序列的疏水性比野生型高1.5倍,但我们发现,如果引入另一种降低gC信号序列总体疏水性的改变,则该缺陷可以在很大程度上得到纠正。我们认为真核信号序列可能存在疏水性上限;超过该值可能导致输出缺陷。