导致 PhiX174 突变体通过磷酸化感染大肠杆菌能力的机制。
Mechanisms responsible for a PhiX174 mutant's ability to infect Escherichia coli by phosphorylation.
机构信息
Department of Biology, Loyola University Chicago, 1032 W. Sheridan, LSB 317, Chicago, IL 60660, USA.
出版信息
J Virol. 2010 May;84(9):4860-3. doi: 10.1128/JVI.00047-10. Epub 2010 Feb 10.
Abstract
The ability for a virus to expand its host range is dependent upon a successful mode of viral entry. As such, the host range of the well-studied PhiX174 bacteriophage is dictated by the presence of a particular lipopolysaccharide (LPS) on the bacterial surface. The mutant PhiX174 strain JACS-K, unlike its ancestor, is capable of infecting both its native host Escherichia coli C and E. coli K-12, which does not have the necessary LPS. The conversion of an alanine to a very reactive threonine on its virion surface was found to be responsible for the strain's expanded host range.
摘要
病毒扩大宿主范围的能力取决于其成功进入宿主的模式。因此，研究充分的 PhiX174 噬菌体的宿主范围由细菌表面特定的脂多糖（LPS）决定。与祖先不同，突变型 PhiX174 菌株 JACS-K 能够感染其天然宿主大肠杆菌 C 和不具有必要 LPS 的大肠杆菌 K-12。在其病毒粒子表面将丙氨酸转换为非常活泼的苏氨酸被发现是该菌株扩大宿主范围的原因。
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