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乳球菌936种噬菌体对乳酸乳球菌表面的附着

Lactococcal 936-species phage attachment to surface of Lactococcus lactis.

作者信息

Geller B L, Ngo H T, Mooney D T, Su P, Dunn N

机构信息

Department of Microbiology, Oregon State University, Corvallis, OR 97331, USA.

出版信息

J Dairy Sci. 2005 Mar;88(3):900-7. doi: 10.3168/jds.S0022-0302(05)72756-9.

Abstract

The interactions of the 936-species phages sk1, jj50, and 64 with the cell surface of Lactococcus lactis LM0230 were analyzed. Cell envelopes (walls + plasma membrane), cell wall, or plasma membrane from L. lactis ssp. lactis LM0230 each inactivated the phages in vitro. However, other 936-species phages kh and P008, which do not infect strain LM0230, were not inactivated by any of the subcellular fractions. Treating cell walls or plasma membrane with the cell wall hydrolase mutanolysin eliminated inactivation of phage sk1. This suggested that intact cell wall fragments were required for inactivation. A role for plasma membrane in phage sk1 inactivation was further investigated. Boiling, washing in 2 M KCl, 8 M urea, or 0.1 M Na(2)CO(3)/pH 11, or treating the plasma membrane with proteases did not reduce adsorption or inactivation of phage. Adding lipoteichoic acid or antibodies to lipoteichoic acid did not reduce inactivation of phage in a mixture with membrane, suggesting that lipoteichoic acid was not involved. Inactivation by envelopes or cell wall correlated with ejection of DNA from the phage sk1 capsid. Although calcium is required for plaque formation, it was not required for adsorption, inactivation, or ejection of phage DNA by envelopes or cell wall. The results suggest that at least for phages sk1, jj50, and 64, adsorption and phage DNA injection into the host does not require a host membrane protein or lipoteichoic acid, and that cell wall components are sufficient for these initial steps of phage infection.

摘要

分析了936型噬菌体sk1、jj50和64与乳酸乳球菌LM0230细胞表面的相互作用。乳酸乳球菌亚种乳酸乳球菌LM0230的细胞包膜(细胞壁+质膜)、细胞壁或质膜在体外均可使这些噬菌体失活。然而,其他不感染菌株LM0230的936型噬菌体kh和P008不会被任何亚细胞组分失活。用细胞壁水解酶变溶菌素处理细胞壁或质膜可消除噬菌体sk1的失活。这表明完整的细胞壁片段是失活所必需的。进一步研究了质膜在噬菌体sk1失活中的作用。煮沸、用2M KCl、8M尿素或0.1M Na₂CO₃/pH 11洗涤,或用蛋白酶处理质膜,均不会降低噬菌体的吸附或失活。添加脂磷壁酸或脂磷壁酸抗体不会降低与膜混合时噬菌体的失活,这表明脂磷壁酸不参与其中。包膜或细胞壁引起的失活与噬菌体sk1衣壳中DNA的释放相关。虽然噬菌斑形成需要钙,但包膜或细胞壁对噬菌体DNA的吸附、失活或释放并不需要钙。结果表明,至少对于噬菌体sk1、jj50和64,吸附和噬菌体DNA注入宿主不需要宿主膜蛋白或脂磷壁酸,并且细胞壁成分足以完成噬菌体感染的这些初始步骤。

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