The Effect of Bacteriophages on Host Physiology
I’ve just come back from a great meeting here at the University of Leicester today, sponsored by the Society for Applied Microbiology and the Society for General Microbiology. Most bacterial genomes are found to contain either whole, or remnants of phage genomes, the expression of which can have a major impact on bacterial physiology. Similarly many phage genomes have acquired key bacterial genes which may be expressed either during a prolonged lytic period or during lysogeny.
Martha Clokie, University of Leicester, who organized the meeting, started off the day with an overview of the current resurgence of interest in the importance of bacteriophages to bacterial behaviour.
The phage takeover of cyanobacterial photosynthetic machinery in the marine environment Jinyu Shan, University of Warwick.
Cyanobacteria such as Synechococcus are obligate phototrophs which generate the energy they need via light-harvesting complexes called phycobilisomes, containing the protein phycoerythrin. When bacteriophage S-PM2 infects Synechococcus, the levels of phycoerythrin increase. This is due to a phage gene called cpeT which increases phycoerythrin gene expression. This could be good for the cells (more energy), and hence good for the phage. Alternatively, the increase in light harvesting could act as a molecular sunscreen, protecting phage from harmful ultraviolet light while still allowing the host cell to harvest energy.
Development of a microarray to study gene expression of the cyanophage S-PM2 during an infection cycle Andrew Millard, University of Warwick.
An array consisting of 5200 spots, representing 300 phage genes, has been used to analyze gene expression in Synechococcus cells infected with phage S-PM2. This has allowed the identification of immediate-early,early, late, etc phage genes. Interestingly, unlike in phages such as coliphage T4, where host cell gene expression is rapidly degraded by phage infection, S-PM2 actually increases expression of a number of host cell genes.
There’s more than one way to kill an E. coli – Bdellovibrio predation! Liz Sockett, University of Nottingham.
Bdellovibrio are facultative intracellular prasites of Gram-negative bacteria. After attaching to the cell, they create an infection pore which allows them to enter the periplasm where replication occurs. The length of the lytic cycle is 1-4 hours, after which about four new Bdellovibrio cells are released. Since the Bdellovibrio genome is ~3.8 megabase pairs, this represents an amazing conversion of host cell cytoplasm into Bdellovibrio DNA. Flagellar mutants of normally highly motile Bdellovibrio (capable of swimming at 160 cell lengths per second) show that entry into the host cell occurs by pili rather than by mechanical burrowing. Bdellovibrio are non-pathogenic to humans and may be part of the normal human flora, so they are under investigation as living antibiotics, particularly for surface infections such as ulcers and pressure sores. Unlike bacteriophages, there is no genetic resistance to infection since there is no simple host cell receptor!
Phage subversion of host metabolism: mechanisms of phage transcription
initiation Debbie Hinton, National Institute of Health, Bethesda, Maryland, USA.
The sigma (s) factor tells bacterial RNA polymerase where to start transcription. Bacteriophages such as coliphage T4 use host cell RNA polymerase to express phage genes. By modifying sigma factors, phage control early, middle and late phases of gene expression.
Construction of a recombinant lambda phage that exhibits selective lethality towards resistant bacteria Barbara Rieck, University of Leicester.
Barbara described attempts to construct antisense resistance genes directed against the lambda cI repressor gene.
Beta-lactam induction of stx2 transcription in Shiga toxin-producing E. coli is RecA dependant Rebecca Smith, University of Leicester.
The Shiga toxins produced by STECs (Shiga Toxin Producing Escherichia coli) such as E. coli O157:H7 are encoded by lysogenic bacteriophages. There are two stx toxins, stx1 and stx2. Stx2 is encoded by two genes, stx2A and stx2B. The host cell SOS response induces the lytic cycle of the lysogenic toxin-carrying phages. Fluoroquinolone antibiotics result in a thousand-fold increase in toxin expression, and some beta-lactam antibiotics also increase stx toxins. This does not occur in RecA mutant
host cells.
Mu-like prophage and their involvement in driving Campylobacter genome evolution Andrew Scott, University of Nottingham.
Phage therapy is being used to reduce Campylobacter infections
in chickens, but the bacteria rapidly develop resistance to the phage. Under phage pressure, Campylobacter undergos extensive genome rearrangements due the the presence of multiple Mu-like prophages.
Evolution of host physiology in response to phage attack Maggie Smith, University of Aberdeen.
The receptor for phage C31 of Streptomyces coelicolor is an unknown glycoprotein. Mutations in the bacterial glycosylation pathway result in resistance to phage infection. S. coelicolor also has a novel restriction modification system called Pgl which is being characterized.
Detecting changes in bacterial cell surface structure using phage interactions Cath Rees, University of Nottingham.
Salmonella phage BP shows serovar-specific host tropism. Conversely, phage infection can cause changes in host cell serotype.
When is a phage not a bacteriophage? When it infects an Archaea: sequences of halophilic archaeal viruses Shaun Heaphy, University of Leicester.
There are only approximately 40 viruses of Archaea described, compared with thousands of bacteriophages and viruses of eukaryotes. Two novel archaeal viruses have been characterized, BJ1 and BJ2. These may become a valuable tool for investigating the biology of Archaea.
What a great day!
Not just what a great day, but what a great collection. :) I loved especially the first animation. Nice work…