Journal of Experimental Microbiology and Immunology (JEMI) Vol. 7:62-67
Copyright © April 2005, M&I UBC
Roles of Lipopolysaccharide and the Outer Membrane Protein OmpC on
Bacteriophage T4 Infectivity in Escherichia coli
WILEY CHUNG, JOHN SIU, KATE TANNER
Department of Microbiology and Immunology, UBC
Although previous studies have demonstrated that lipopolysaccharide (LPS) and the
outer membrane protein OmpC are required for bacteriophage T4 infectivity in
Escherichia coli, it is unclear whether they played a role in binding or in the downstream
viral processes that followed. Such processes may vary from phage DNA injection to viral
gene expression, assembly, or release. To investigate this further, phage binding and
overlay plaque assays were performed on E. coli strains C149 (wildtype), C845 (LPS
mutant), C842 (LPS mutant), and C157 (OmpC mutant). In this study, we report that LPS
and OmpC play an essential role in one or more viral processes that follow binding. In
addition, it was discovered that LPS and OmpC mutants C842 and C157, respectively, did
not alter phage binding affinity but decreased phage binding stability. Moreover, the LPS
mutant, C845, increased binding affinity to T4 phage but decreased binding stability. All
these results suggest that modifications to LPS can influence both the affinities and
stabilities of phage binding.
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The T4 bacteriophage, a member of the T-even
phage group, is an efficient infectious agent of
Escherichia coli (E. coli) (4). Its structure consists of a
DNA-containing head, a tail, as well as a baseplate
which is attached to both short and long tail fibres (12).
T4 phage employ a very complex entry mechanism,
involving an ATP-dependent DNA injection process
(7). Bacteriophages remain attached to the outer cell
surface during infection and have evolved a mechanism
to use their tail fibers for host cell recognition,
attachment, and genome delivery (7).
T4 phage contain six tail fibers which are
symmetrically organized around a hexagonal baseplate
(1,3). Initial attachment to a host cell receptor is
reversible, weak, and dependent upon the interaction
between at least three long tail fibers and a glucose
residue on of the outer core of the lipopolysaccharide
(LPS) of the host cell surface (1). Previous studies
have shown that these binding interactions are weak
and may vary from hydrogen bonding to hydrophobic
and electrostatic interactions (4). After the tail fiber
binding has been consolidated, the baseplate then
comes in contact with the host cell surface, causing the
short tail fibers to eject and bind irreversibly to the
heptose section of the inner core of the LPS (1). This
transition from reversible to irreversible binding
involves a number of host and phage components (3,7).
After this conformational change, the tail sheath
contracts, causing the tail tube to be forced through the
outer cell membrane of the host (1). The tail tube then
reaches the inner membrane, aided by the tail
lysozyme, glycoprotein 5. The phage genome is then
injected into the host cytoplasm (1). It is important to
note that the irreversibly bound state can exist in two
phases, one where the phage DNA has not been
internalized and one where it has. Following DNA
injection, the host cell transcription and translation
machinery is used to produce phage specific early
mRNA and proteins (1). Eventually, late mRNA and
proteins are produced (1). These proteins include
phage structural proteins as well as proteins involved in
cellular lysis (1). Ultimately, infectious phage particles
are assembled and the host cell undergoes lysis and
releases phage progeny (11).
Previous studies have demonstrated that LPS and
the outer membrane protein OmpC are required for
bacteriophage T4 infectivity in E. coli (9,11,12). LPS
is located exclusively in the outer leaflet of the outer
membrane of gram negative bacteria (11). LPS
exhibits features of both lipids and polysaccharides and
its structure is divided into three regions: Lipid A, R-
core, and O-polysaccharide (11). OmpC is an outer
membrane protein that is involved in regulating the
response of E. coli to the osmolarity of its environment
(2). It is highly expressed during conditions of high
osmolarity and repressed during conditions of low
osmolarity (2). Particular studies found that E. coli K-
12 strains that contained a mutation in their OmpC or
LPS structures were resistant to T4 phage infection
(9,12). Although these studies have helped identify
that both LPS and OmpC are required for infectivity, it
was unclear whether these structures played a role in
binding or in downstream viral processes that followed.
Such processes may vary from phage DNA injection to
viral gene expression, assembly, or even release.
The purpose of this experiment was to determine
whether LPS and OmpC are involved in the initial
binding of phage or a viral process that followed
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