Growth, Differentiation and Sexuality

and Hamer 1998; Harris et al. 1999; Momany et al.
1999; Shi et al. 2004). Deletion of hypA results in
swollen hyphae which lyse, abnormal conidia and
nuclear defects. In addition, the ΔhypA and hypA1
mutant strains showed decreased secretion of amylose,
disorganisation of endomembranes and loss
of the Spitzenkörper (an apical cluster of vesicles
and cytoskeletal elements visible at the cell apex),
which suggests a role in the secretory pathway (Shi
et al. 2004).
C. Polarised to Isotropic Growth
1. Budding
After bud emergence in S. cerevisiae,aswitchfrom
polarisedgrowthtoisotropicgrowthoccurs,allowingthebudtogrowinalldirections.Thistransition
involvesthehydrolysisofGTPboundtoCdc42p,
catalysed by one or more GTPase activating proteins,
and results in the phosphorylation of Gic2p,
the PAK Cla4p and the cell cycle-associated protein
Gin4p, thereby effecting the switch from apicalgrowthofthebudtoisotropicgrowth.This
growth switch also depends on the activation of the
complex containing the cyclins Clb1p and Clb2p,
and the cyclin-dependent kinase (CDK) Cdc28p, as
bud morphogenesis is coupled to cell division control.
Bud emergence is followed by the formation of
an actomyosin contractile ring at the mother–bud
junction, cytokinesis and cell separation (reviewed
in Johnson 1999).
2. Appressorium Peg
During infection, hyphae of plant pathogens
differentiate specialized infection structures
called appressoria. Appressoria are formed by the
swelling of the germ tube tip (analogous to a switch
from polarised growth to isotropic growth) when
the appropriate signal(s) are received from the
plant surface. Subsequently, formation of the
penetration peg which enters the plant requires an
isotropic to polarised switch. Unfortunately, little is
known about the role of cell polarity determinants
in appressorium formation. It has been shown in
thericepathogenMagnarporthe grisea that cAMP
signalling regulates appressorium formation
(Xu and Hamer 1996). In addition, a number of
MAPKs have been identified in M. grisea which
are required for appressorium formation and
cell wall integrity, including Pmk1 (homologue
of S. cerevisiae Fus3p), Mps1 (homologue of S.
Generating Fungal Cell Types 15
cerevisiae Slt2p), Mst7 and Mst11 (homologues of
S. cerevisiae Ste7p MEK and Ste11p MEKK) (Xu
et al. 1993; Xu and Hamer 1996; Xu et al. 1998;
Zhao et al. 2005). The RAS homologue C. trifolii is
also required for polarised growth of hyphae and
appressoria formation (Memmott et al. 2002).
3. Conidiophore Production
Many mycelial fungi produce asexual spores
on specialized cellular structures termed conidiophores
(see Chap. 14, this volume). The
development of conidiophores requires the differentiation
of morphologically distinct cell types
from the vegetative mycelium, and thus changes in
polarised growth. In A. nidulans, the conidiation
process begins with the growth of a conidiophore
stalk by apical extension from a thick-walled
vegetative cell termed a foot cell (Fig. 1.9). The tip
of the stalk then undergoes an apical to isotropic
switch to produce the conidiophore vesicle. The
foot cell, stalk and vesicle are not separated by
septa. A layer of uninucleate cells termed metulae
bud from the vesicle, and these metulae then bud
from their distal end to produce uninucleate cells
termed phialides, in a process analogous to polar
budding in S. cerevisiae. Repeated asymmetric
divisions by phialides produce chains of uninucleate
conidia (Adams et al. 1998). The central
regulatory pathway controlling asexual development
includes three genes specifically required for
conidiation, brlA, abaA and wetA (Adams et al.
1988; Mirabito et al. 1989). These gene products
control conidiation-specific gene expression and
the order of gene expression during conidiophore
development. Two other developmental genes,
stuA and medA, are necessary for the spatial
pattern of the conidiophore (Adams et al. 1998).
The central regulatory pathway is inhibited by
a G-protein-mediated signalling pathway (Adams
et al. 1998). The small GTPase RasA also regulates
the onset of asexual development in A. nidulans,
independently of the G-protein signalling pathway
(Som and Kolaparthi 1994). Although the morphology
of P. marneffei conidiophores differs from
that of A. nidulans, the molecular mechanisms
which control this developmental program are
conserved (Zuber et al. 2002; Boyce et al. 2005).
How changes in polarity are mediated during
asexual development in mycelial fungi remains
largely unknown. Similarly to other developmental
pathways, some of the key components required
for polarity establishment and maintenance have