Biology Reference
In-Depth Information
to differences in life style, time since the Ýrst infection, and order of gene loss. For example,
the
Buchnera
lineages of Lachninae may have deleted a more substantial fraction of their genomes
prior to the loss of the
recA
gene. Or, alternatively, their evolution may have been faster than
that of the other genomes.
INTRACELLULAR MUTUALISM VS. PARASITISM
It is conceivable that the colonization of an intracellular environment, whether leading to a mutu-
alistic or a parasitic relationship, is based on a common strategy. This is reÞected in a number of
shared genomic features that appear to be characteristic of bacteria that reproduce in a host-
associated manner: small genome sizes when compared to their free-living relatives, a reduced
gene repertoire, absence of extensive repetitive elements, and a tendency toward AT richness.
Possible explanations for the increase in AT content are a reduced capacity to repair misinsertions
of thymidine and adenine into DNA via replication errors and C to U deaminations. The use of
similar invasion strategies is also reÞected by a certain amount of damage, which in some cases is
inÞicted on a host not only by pathogens but also at early stages of colonization by the intracellular
mutualists. In addition, elevated production of stress-related proteins in both intracellular parasites
and mutualists has been observed (Goebel and Gross, 2001).
Nevertheless, the genomes of mutualists and parasites, though both well suited for intracellular
existence, do show characteristic differences that arise from the particular lifestyles of the organ-
isms. Although there is a general loss of genes involved in regulation, biosynthesis, and repair and
recombination processes (and to a lesser extent in energy metabolism and basic cellular processes)
in both organisms, speciÝc parts of the metabolic systems are often preserved or even ampliÝed in
the endosymbionts.
This may not be surprising because the eukaryote provides a stable and isolated environment
that is also rich in nutrients, while the bacteria are expected in return to produce nutrients desired
by the host. The effect is that genes associated with these desired metabolic pathways are under
particularly high selective pressure. As a result, in addition to their being maintained in the genome,
their functions may even be improved or altered according to the demands of the host. This is
observed in
Buchnera
for genes associated with the biosynthesis of amino acids. For example, the
trpEG
genes have been relocated and subsequently ampliÝed on plasmids to escape feedback
inhibition. In contrast, intracellular pathogens such as
Rickettsia
have lost most genes dedicated to
biosynthetic functions because the corresponding metabolites are present and easily accessible in
the host cell. Other differences observed between
Rickettsia
and
Buchnera
include the lack of a
glycolytic system in
R. prowazekii
(Andersson et al., 1998) and of the TCA cycle in
Buchnera
(Shigenobu et al., 2000; Tamas et al., 2002).
In parasites, the loss of basic biosynthetic capabilities is often complemented by elevated
exportÏimport capabilities. Moreover, the presence of pathogenicity-related genes in parasites is
necessary for ensuring the invasion of the host cell. This functional category is largely eliminated
from genomes of obligate intracellular mutualists, such as
Buchnera
spp. Those few
Buchnera
genes, which according to homology searches should be classiÝed as virulence factors, are probably
either functionally altered or simply required for entry into the host cell. For example, genes
encoding Þagellar structures, typically used for bacterial motility, have atypically high substitution
rates and may have evolved a novel function (transport) in
Buchnera
due to the mutualistic lifestyle
(Tamas et al., 2002).
Also in contrast to parasites, a reduced repertoire of genes encoding cell-surface structures has
been observed in
Buchnera
. Such a loss is not an option for parasites, which utilize cell-surface
proteins for continued virulence. Intracellular pathogens like
R. prowazekii
must penetrate host
defense mechanisms to gain access to the intracellular environment. Here, cell-surface structures
are assumed to play a prominent role.
