甘氨酸113突变为天冬氨酸可恢复大肠杆菌蜜二糖载体中天冬氨酸51突变为丝氨酸的突变体的活性。
GLY113-->ASP can restore activity to the ASP51-->SER mutant in the melibiose carrier of Escherichia coli.
作者信息
Wilson D M, Hama H, Wilson T H
机构信息
Department of Cell Biology, Harvard Medical School, Boston, MA 02115, USA.
出版信息
Biochem Biophys Res Commun. 1995 Apr 6;209(1):242-9. doi: 10.1006/bbrc.1995.1495.
ASP51 in the putative membrane-spanning helix 2 of the melibiose carrier of Escherichia coli was replaced by SER. This mutation caused failure of the cell to transport melibiose and failure to ferment melibiose on indicator plates. A melibiose-positive revertant was isolated from these plates and was found to have two additional mutations, GLY113-->ASP (in helix 4) and PHE16-->LEU (in helix 1). The double mutant ASP51-->SER/GLY113-->ASP was constructed and showed accumulation of melibiose. On the other hand ASP51-->SER/PHE16-->LEU showed no activity. It is concluded that the new carboxyl group at position 113 compensates for the loss of the carboxyl group at position 51.
将大肠杆菌蜜二糖载体假定的跨膜螺旋2中的ASP51替换为SER。该突变导致细胞无法转运蜜二糖，且在指示平板上无法发酵蜜二糖。从这些平板中分离出一株蜜二糖阳性回复体，发现其还有另外两个突变，GLY113→ASP（在螺旋4中）和PHE16→LEU（在螺旋1中）。构建了双突变体ASP51→SER/GLY113→ASP，其表现出蜜二糖积累。另一方面，ASP51→SER/PHE16→LEU没有活性。得出的结论是，113位上新的羧基补偿了51位羧基的缺失。
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