| Abstract |
This study focus in the mosquito stages of malaria parasites. The results are
presented in four chapters. The first chapter describes the mechanism of gametocyte
egress from the host erythrocyte during gametogenesis. Malaria parasites infect
erythrocytes and initiate a series of asexual multiplication cycles or they develop into
female and male gametocytes. The production of female and male gametes, known as
gametogenesis, takes place after uptake by the mosquito. The parasite egress from the
host erythrocyte during gametogenesis involving sequential rupture of the membranes
of the parasitophorous vacuole (PVM) and erythrocyte (RBCM). We present detailed
observations of these events in real time using high-speed video microscopy and
immunofluorescence assays. The first sign of egress is swelling of the host cell. The
PVM ruptures and vesiculates. This is followed by the opening of a single stabilized
pore of the RBCM. The RBCM is subsequently vesiculated, releasing the gametes. In
the second chapter we study actin 2, one of the two actin isoforms in malaria parasites.
Actin 1 has a vital role in all developmental stages, whereas actin 2 is essential in male
gametogenesis. By genetic replacement of actin 2 with actin 1, we show that the two
actin isoforms have distinct functions in male gametogenesis and we found an
additional essential role of actin 2 in oocyst development. The function of actins
depends on the polymerization properties. In the third chapter, replacement of actin 2
by chimeric actin 1 revealed that polymerization of actin 2 is necessary in
gametogenesis but is not enough for the oocyst development. In the fourth chapter,
global expression profiling reveals shared and distinct transcript signatures in arrested
act2(-) and CDPK4(-) gametocytes.
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Γαμετογένεση και μελέτη της ακτίνης 2 στα παράσιτα της ελονοσίας
