Biology Reference
In-Depth Information
gametes, a process that requires among much else cGMP-dependent protein kinase
signaling and NIMA-related kinases (Reininger et al.
2005
,
2009
; McRobert et al.
2008). Most impressive is the formation of the male gamete, within the host cell
cytoplasm. After three rapid rounds of genome replication, followed by three
endomitoses, eight flagellated gametes are formed in a process that somehow
requires a specific actin isoform, actin II (Siden-Kiamos et al.
2011
). The flagella
in gametes consist of alpha tubulin II, which like actin II is specifically expressed
at this stage. The small differences between the two isoforms of actin and tubulin
thus may be essential for their specific role in exflagellation and gamete motility
(Rawlings et al.
1992
). Male-gametes of Toxoplasma also exflagellate in the sexual
phase in cats. However, Toxoplasma only has one copy of alpha and beta tubulin
(Nagel and Boothroyd
1988
). However, due to the intrinsic difficulty to work with
Toxoplasma sexual forms (in cats), little is known about the molecules and
mechanisms of male-gamete formation. The axonemes of plasmodium flagella are
derived from eight kinetosomes (acting like basal bodies) that in turn originate
from a single, amorphous MTOC, located at a nuclear pore (Sinden et al. 1976,
2010
). Important for this is an atypical mitogen-activated protein kinase, required
to start cytokinesis and axoneme motility (Tewari et al.
2005
). Eventually the
gametes escape from the host cell and, propelled by their flagella, zoom at high
speed through the mosquito stomach cavity, to find and fuse with a female gamete.
19.2.2 Toxoplasma
Toxoplasma gondii is an obligate intracellular pathogen able to infect and replicate
in most nucleated cells of warm-blooded animals. It is the etiologic agent of
toxoplasmosis, one of the most common parasitic infections in humans, with a
worldwide distribution, chronically infecting approximately one-third of the world
population. In most adults toxoplasmosis is asymptomatic. But in some individ-
uals, it can cause blindness and in embryos infected maternally during pregnancy
even mental retardation and death.
The life cycle of Toxoplasma has an asexual phase, which takes place in most
animals, and a sexual phase in felids (cats), with three distinct infective forms.
The asexual cycle comprises two distinct parasite forms. The rapidly replicating
form is responsible for the clinical manifestations of acute toxoplasmosis
(Fig.
19.4
a). With the activation of the inflammatory response by the host, the
parasite differentiates into a tissue cyst form, where both multiplication and
metabolism are slowed down.
Both the faster and the slower replicating forms divide by the same process,
called endodyogeny, a specialized system of reproduction where two daughter
cells are formed within a mother cell (Fig.
19.4
b - d). In contrast to the schizogony
of Plasmodium, this unique form of division allows the parasite to remain infective
during the division process. At the beginning of endodyogeny, the parasite elon-
gates and widens the Golgi apparatus and apicoplast. This is followed by the
