Alexander J E, Andrew P W, Jones D, Roberts I S
Department of Microbiology, University of Leicester, United Kingdom.
Infect Immun. 1993 May;61(5):2245-8. doi: 10.1128/iai.61.5.2245-2248.1993.
A transposon insertion mutant of Listeria monocytogenes was shown to be deficient in prephenate dehydratase, an enzyme acting late in the pathway for biosynthesis of phenylalanine. This mutant had reduced virulence in mice. The mutant and parent strains persisted to the same extent in the tissues of infected mice and elicited similar degrees of splenomegaly. Mice vaccinated with the mutant were protected significantly from subsequent challenge with virulent L. monocytogenes.
一株单核细胞增生李斯特菌的转座子插入突变体被证明缺乏预苯酸脱水酶,该酶在苯丙氨酸生物合成途径中起后期作用。此突变体在小鼠中的毒力降低。突变体菌株和亲本菌株在感染小鼠组织中的存留程度相同,并引起相似程度的脾肿大。用该突变体疫苗接种的小鼠受到显著保护,免受随后强毒单核细胞增生李斯特菌的攻击。