Busch C, Hofmann F, Selzer J, Munro S, Jeckel D, Aktories K
Institut für Pharmakologie und Toxikologie der Albert-Ludwigs-Universität Freiburg, Hermann-Herder-Str. 5, D-79104 Freiburg, Germany.
J Biol Chem. 1998 Jul 31;273(31):19566-72. doi: 10.1074/jbc.273.31.19566.
A fragment of the N-terminal 546 amino acid residues of Clostridium sordellii lethal toxin possesses full enzyme activity and glucosylates Rho and Ras GTPases in vitro. Here we identified several amino acid residues in C. sordellii lethal toxin that are essential for the enzyme activity of the active toxin fragment. Exchange of aspartic acid at position 286 or 288 with alanine or asparagine decreased glucosyltransferase activity by about 5000-fold and completely blocked glucohydrolase activity. No enzyme activity was detected with the double mutant D286A/D288A. Whereas the wild-type fragment of C. sordellii lethal toxin was labeled by azido-UDP-glucose after UV irradiation, mutation of the DXD motif prevented radiolabeling. At high concentrations (10 mM) of manganese ions, the transferase activities of the D286A and D288A mutants but not that of wild-type fragment were increased by about 20-fold. The exchange of Asp270 and Arg273 reduced glucosyltransferase activity by about 200-fold and blocked glucohydrolase activity. The data indicate that the DXD motif, which is highly conserved in all large clostridial cytotoxins and also in a large number of glycosyltransferases, is functionally essential for the enzyme activity of the toxins and may participate in coordination of the divalent cation and/or in the binding of UDP-glucose.
索氏梭菌致死毒素N端546个氨基酸残基的片段具有完整的酶活性,且在体外可使Rho和Ras GTP酶发生糖基化。在此,我们鉴定出索氏梭菌致死毒素中的几个氨基酸残基,它们对于活性毒素片段的酶活性至关重要。将第286位或288位的天冬氨酸替换为丙氨酸或天冬酰胺,可使糖基转移酶活性降低约5000倍,并完全阻断葡萄糖水解酶活性。双突变体D286A/D288A未检测到酶活性。索氏梭菌致死毒素的野生型片段在紫外线照射后可被叠氮基 - UDP - 葡萄糖标记,而DXD基序的突变则阻止了放射性标记。在高浓度(10 mM)的锰离子存在下,D286A和D288A突变体的转移酶活性增加了约20倍,而野生型片段的转移酶活性未增加。Asp270和Arg273的替换使糖基转移酶活性降低约200倍,并阻断了葡萄糖水解酶活性。数据表明,DXD基序在所有大型梭菌细胞毒素以及大量糖基转移酶中高度保守,对毒素的酶活性在功能上至关重要,可能参与二价阳离子的配位和/或UDP - 葡萄糖的结合。