Biology Reference
In-Depth Information
copy of the organelle during mitosis. As discussed above, in schizogony when
dozens of budding cells are formed at the same time, the apicoplast and the
mitochondrion enlarge and then segment, being later directed to the budding cells.
Is this apicoplast-mitochondrion-nucleus connection a common strategy to assure
each daughter cell a copy of the organelle? Or perhaps each apicomplexan
developed its own mechanisms? These are questions that still require further
studies.
Until recently, it was poorly understood how daughter cells acquired the
complete set of chromosomes after the sequential division process. Brooks et al.
(
2011
) recently demonstrated that the parasite's chromosomes are connected to the
centrosome throughout the cell cycle, allowing the correct distribution during
daughter cell budding. They followed a component of the chromosomes' centro-
meres—CenH3—throughout the cell cycle to characterize the chromosomal
architecture during mitosis. This centromere associates with the centrocone during
both mitosis and interphase, allowing genome integrity during rapid DNA repli-
cation and re-location to budding cells.
Toxoplasma reorganizes host cell intracellular structures, like lysosomes,
mitochondria, endoplasmic reticulum, and the Golgi in order to acquire nutrients
for its intracellular development. Curiously, Toxoplasma also reorganizes the host
cell centrosomes. The mammalian target of rapamycin signaling pathway
(mTOR), a highly conserved serine/threonine kinase, is a key controller of cell
growth and proliferation (Zoncu et al.
2011
). It has been shown as well that
mTORC2 is important for cell polarity control, actin organization, and stimulation
of F-actin stress fibers (Schmidt et al.
1996
; Sarbassov et al.
2005
). By meddling
with the protein mTORC2 the parasite interferes with host centrosome location,
re-directing it to the parasitophorous vacuole and suppressing host cell migration
(Wang et al.
2010
). Interfering with the polarization of the host cell microtubules
may lead to an arrest of the host cell in a state favorable for the intracellular
development of the parasite.
19.2.3 Theileria
Theileria is another unique apicomplexan parasite, being an important pathogen
for cattle in Africa and Asia. After infecting the immune system's cells (i.e.
macrophages or lymphocytes), Theileria induces an uncontrolled proliferation of
these cells by recruitment of IKK onto the parasite surface and thus activation of
NFkB, effectively turning them into cancer cells (Heussler et al.
2002
). The
infected host cells do not undergo apoptosis and can survive for years (Küenzi
et al.
2003
; Heussler et al.
2006
;). Infected cells migrate across tissue barriers and
establish new areas of proliferation, especially in the lymphoid tissue (reviewed by
Baumgartner
2011
). In the laboratory, Theileria infected cells can be cultivated
and experiments probing parasite infection are done ''in reverse'', not by infecting
uninfected host cells, but by curing infected ones.
