Introduction to Fungi, Third Edition

PNEUMOCYSTIS
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formation of the intranuclear spindle (Hagan,
1998). No further cell wall extension takes
place during mitosis, presumably because no
cytoplasmic microtubules are available to drive
it. By contrast, actin relocates from the poles to
the centre of the cell, forming a ring around
the equator in close proximity to the nucleus
(Figs. 9.6c,d). Actin aggregation is co-ordinated
by a protein (Mid1p) emitted from the nucleus
to form a broad cortical band, which in turn
is controlled by the activity of the nuclear protein
kinases Plo1p and Pdk1p (Bähler et al., 1998;
Brunner & Nurse, 2000; Bimbó et al., 2005).
Since the positioning of the nucleus in the
cell is determined by microtubules, these are
ultimately responsible for morphogenesis in
S. pombe. Microtubules pull apart the two
daughter nuclei (Figs. 9.6d,e), and when these
have reached the two opposite poles (Fig. 9.6e),
the spindle breaks down and the basket of
cytoplasmic microtubules is re-established (Fig.
9.6f). Meanwhile, the actin ring co-ordinates the
inward growth of the septum wall. When the
septum has been completed, actin relocates to
the two old ends, one in each daughter
cell, which resume growth (Figs. 9.6g,h). It is
remarkable that the septum is laid down
precisely in the middle of a cell which was
itself synthesized by asymmetric elongation of
its two ends.
If a cell of S. pombe comes into close proximity
to a cell of opposite mating type and is in the G1
phase prior to the START point, it will conjugate.
The formation of a projection tip during conjugation
requires the presence of actin for localized
cell wall synthesis and lysis, and microtubules
to localize actin towards this new if transient
growing point (Petersen et al., 1998). Cell-to-cell
fusion also requires the accumulation of actin
(Kurahashi et al., 2002).
9.4 Pneumocystis
This is an unusual but appropriately named
group of organisms living as cyst-like cells in
the lungs of mammalian hosts, where they
cause pneumonia in immunocompromised
individuals. The identity of these organisms as
fungi was established beyond doubt only relatively
recently, following DNA sequence comparisons.
Recently, these techniques have also
permitted the distinction between different
taxonomic entities within Pneumocystis which
correlate with the taxonomy of their hosts.
Thus, the original name P. carinii is now applied
by most workers only to a species infecting rats,
with the human pathogen called P. jirovecii
(Stringer et al., 2002).
Little is known about the life cycle of
Pneumocystis because this organism cannot
be grown satisfactorily outside its host. Cushion
(2004) summarized evidence indicating that
there is probably a haploid trophic phase in
which cells divide by binary fission in an amoebalike
way, i.e. by constriction. Trophic cells of
Pneumocystis are firmly attached to mammalian
pneumocyte I cells in the alveolar regions of
lung tissue. The cell wall of the trophic stage
is unusually thin and flexible. If two compatible
trophic cells fuse, a diploid zygote is formed
and undergoes meiosis, producing a thick-walled
cyst containing eight ascospores which are
presumed to develop into a fresh crop of trophic
cells upon germination. Pneumocystis can
cause lethal pneumonia in immunocompromised
hosts and the pneumonia it causes is
regarded as an AIDS-defining illness. Infections
have also been linked with the sudden infant
death syndrome, reflecting contact of children
with Pneumocystis very soon after birth. Exposure
to inoculum seems to have little effect on
immunocompetent individuals, although there
is evidence that they may carry latent Pneumocystis
infections of limited duration. Considerable
uncertainty exists about the epidemiology
of Pneumocystis. Although there have been occasional
reports of the detection of P. jirovecii
DNA in nature, there is no convincing evidence
of any external reservoir of inoculum which
could represent a source of human infections.
The fungus therefore seems to be spread mainly
or exclusively between humans. One way by
which Pneumocystis may avoid the mammalian
immune response is its ability to alter the
properties of surface glycoproteins acting as
antigens.