Biology Reference
In-Depth Information
It is necessary to distinguish between gene loss due to pathoadaption and
due to reductive evolution. The model of reductive evolution is based on the
lack of universal need of some genes across different niches. So, genes that
are essential in one habitat but are not required in a novel habitat could be lost
based on the use-it-or-lose-it principle, especially if the habitat shift is perma-
nent. The latter trajectory of evolution develops when certain bacteria change
their lifestyle to an obligate intracellular pathogen, and permanently shed off
genes non-essential within the host (
Moran and Plague, 2004
).
Mycobacterium
leprae
(
Cole et al., 2001
),
Coxiella burnetii
(
Seshadri et al., 2003
), the Rick-
ettsiae (
Andersson et al., 1998
) are some examples of reductive genome evolu-
tion. Moreover, the restricted intracellular lifestyle within a host reduces the
possibility of HGT events thereby maintaining a reduced genome size (
Moran
and Plague, 2004
). However, loss of gene by such a mechanism is not driven
by positive selection pressures for it, and therefore is not adaptive per se. The
unnecessary genes are either not expressed or their expression does not provide
fitness advantage or significant disadvantage. Thus, their loss rather happens
due to the lack of negative selection against it and is driven by genetic drift and
not positive selection.
Alternatively, loss of certain genes could be highly adaptive, especially for
pathogens. Indeed, genes that are essential for the fitness in one habitat might be
not only useless but also
detrimental
for the fitness in another habitat (
Maurelli,
2007
). This will force the emergence of new variants of the bacterium through
elimination of genes that, for example, down-regulate those genes, increased
expression of which is important for the fitness in the new niche. Another exam-
ple would be elimination of genes, the product of which either directly inhibits
the function of critical traits or provides liability in the new habitat, e.g. those
coding for the surface structure recognized well by innate or adaptive immune
mechanisms.
Genes, the function of which is detrimental to virulence, are sometimes
termed 'antivirulence factors'. A great example of an antivirulence gene is
cadA
in
Shigella
spp. The gene
cadA
encodes lysine decarboxylase (LDC) and is
expressed in >90% of
E. coli
isolates (
Maurelli, 2007
). However, all strains of
Shigella
as well as the enteroinvasive
E. coli
(EIEC that cause dysentery simi-
lar to shigellosis, see Chapter 7) lack expression of LDC (
Silva et al., 1980
).
Experiments in an animal model showed that if
Shigella
was forced to produce
LDC via transformed
cadA
, it remained invasive but its enterotoxic activity was
significantly diminished compared to the wild-type level (
Maurelli et al., 1998
).
The product of lysine decarboxylation is cadaverine, which inhibits the function
of plasmid-encoded enterotoxins in
Shigella
. Another experiment showed the
role of cadaverine in preventing the ability of
Shigella
to stimulate transepi-
thelial migration of polymorphonuclear neutrophils (
McCormick et al., 1999
).
Since expression of LDC followed by production of cadaverine attenuates viru-
lence phenotypes,
cadA
in
Shigella
satisfies the necessary features of an antivir-
ulence gene (
Maurelli, 2007
). Another example of an antivirulence gene, again in
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