Biology Reference
In-Depth Information
FIGURE 13.1
single infections are
indicated by black or gray shading. Superinfection is indicated by black + gray shading. ÑXÒ indicates CI. CI
provides a reproductive advantage to single-infected females relative to uninfected females (unshaded) because
they can mate successfully with more male types. Similarly, superinfected females are at a reproductive
advantage relative to single and uninfected females because they are compatible with all male types. The
reproductive advantage afforded by CI to infected females can result in population replacement, with the
infected cytotype driving into the host population and replacing the uninfected cytotype.
Pattern of egg hatch resulting from additive CI. Differing
Wolbachia
2002b). A general equation (Hoffmann
et al., 1990; Turelli, 1994) describing
Wolbachia
infection
frequency (
p
) at time
t
is given as:
p
t
1
)
Ï
n
*
)
1
Ï
s
f
*
p
t
=
--------------------------------------------------------------------------------------------
(13.1)
+
1
n
s
h
p
t
2
1
Ï
s
f
p
t
Ï
s
h
p
t
1
)
Ï
p
t
*
Ï
)
1
Ï
s
f
*
where (1 Ï
s
) is the proportion egg hatch resulting from CI crosses, (1 Ï
n
) is the Ýdelity of
Wolbachia
h
maternal transmission, and (1 Ï
s
) is
Wolbachia
effects on host fecundity. The speed at which
f
Wolbachia
invades a host population (population-replacement rate) is directly related to the Ýdelity
of maternal transmission and relative fecundity of infected host females and is inversely related to
egg hatch resulting from incompatible crosses. Equation 13.1 may also be used to characterize the
initial infection frequency required for
to invade the host population (threshold infection
frequency) and the equilibrium infection frequency following
Wolbachia
invasion. Infection levels
below the required infection threshold do not invade and are lost from the host population. Additional
models examining infection dynamics include
Wolbachia
Wolbachia
effects on sperm competition (Wade and
Chang, 1995),
Wolbachia
infections that do not cause CI (Hoffmann
et al., 1996), CI-inducing
Wol-
bachia
et al., 2002b), and
natural ÑcuringÒ of infected individuals by heat, naturally occurring antibiotics, and diapause (Stevens,
1989; Karr, 1991; Stevens and Wicklow, 1992; Perrot-Minnot
infections that increase host Ýtness relative to uninfected hosts (Dobson
et al., 1996).
Although the mechanism responsible for CI has not yet been identiÝed, a poison/antidote model
has been used to explain the observed phenomenon (Werren, 1997). In this model, modiÝcation
(
are shed from maturing sperm (Presgraves,
2000). Embryos that are fertilized with modiÝed sperm are arrested in early development unless
the rescue (
mod
) occurs on the male pronucleus, before
Wolbachia
resc
) function is expressed in eggs from
Wolbachia
-infected females. In recent studies
examining cytoplasmically incompatible embryos of
wasps,
researchers have observed a delayed breakdown of the paternally contributed pronuclear envelope
(Callaini
Wolbachia-
infected
Nasonia vitripennis
et al., 1997; Tram and Sullivan, 2002). The observations have led to the postulation that
the resulting asynchrony between the maternal and paternal pronuclei is the primary defect in CI
