Short Noncontractile Tail Machines: Adsorption and DNA Delivery by Podoviruses

Chapter
Part of the Advances in Experimental Medicine and Biology book series (AEMB, volume 726)

Abstract

Tailed dsDNA bacteriophage virions bind to susceptible cells with the tips of their tails and then deliver their DNA through the tail into the cells to initiate infection. This chapter discusses what is known about this process in the short-tailed phages (Podoviridae). Their short tails require that many of these virions adsorb to the outer layers of the cell and work their way down to the outer membrane surface before releasing their DNA. Interestingly, the receptor-binding protein of many short-tailed phages (and some with long tails) has an enzymatic activity that cleaves their polysaccharide receptors. Reversible adsorption and irreversible adsorption to primary and secondary receptors are discussed, including how sequence divergence in tail fiber and tailspike proteins leads to different host specificities. Upon reaching the outer membrane of Gram-negative cells, some podoviral tail machines release virion proteins into the cell that help the DNA efficiently traverse the outer layers of the cell and/or prepare the cell cytoplasm for phage genome arrival. Podoviruses utilize several rather different variations on this theme. The virion DNA is then released into the cell; the energetics of this process is discussed. Phages like T7 and N4 deliver their DNA relatively slowly, using enzymes to pull the genome into the cell. At least in part this mechanism ensures that genes in late-entering DNA are not expressed at early times. On the other hand, phages like P22 probably deliver their DNA more rapidly so that it can be circularized before the cascade of gene expression begins.

Keywords

Phage Genome Tail Fiber Secondary Receptor Tail Protein Enterobacterial Common Antigen 
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.

Notes

Acknowledgments

We thank all our colleagues in this unusually collegial research field for many years of open and insightful discussions. We especially thank our own coworkers for their contributions to our respective research programs, which are supported by NIH grants GM32095 to IJM and AI074825 to SRC.

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© Springer Science+Business Media, LLC 2012

Authors and Affiliations

  1. 1.Division of Microbiology and Immunology, Pathology DepartmentUniversity of Utah School of MedicineSalt Lake CityUSA
  2. 2.Section of Molecular Genetics and Microbiology, Institute for Cellular and Molecular BiologyUniversity of Texas at AustinAustinUSA

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