Growth, Differentiation and Sexuality

eports suggested such a function for the myosin
light chain encoded by MLC1 in S. cerevisiae (Wagner
et al. 2002; Luo et al. 2004). Mlc1p is a light
chain for both Myo1p (in the acto-myosin ring)
and Myo2p (vesicle transport), and also recruits
Iqg1p/Cyk1p to septal sites (Shannon and Li 2000;
Terrak et al. 2003).
Chitin at septa is synthesized by chitin synthases.
In S. cerevisiae, a primary septum can be
distinguished from secondary septa. The primary
septum is laid down during acto-myosin ring constriction,
forms a chitin-rich disk between mother
and bud, and thus leads to the separation of the
mother and daughter cytoplasms. The secondary
septa are then built from both mother and daughter
sides filling the space between the primary septum
and cell membrane (Roncero 2002). The number
of chitin synthases in fungal organisms varies.
In S. cerevisiae three chitin synthases are present,
encoded by CHS1, CHS2, andCHS3, but up to
seven have been reported, for example, in A. fumigatus
(Roncero 2002). There is both temporal as
well as spatial regulation of chitin synthesis. Chs1p
(class I) is a minor chitin synthase that is involved in
repair synthesis of chitin during cytokinesis (Cabib
et al. 1992). Chs2p (class II) is required for primary
septum formation, whereas Chs3p (class IV) is the
major chitin synthase, and contributes chitin synthesis
of the chitin ring and the chitin of the cell wall
during vegetative growth (for details, see Sietsma
and Wessels, Chap. 4, and Latgé and Calderone,
Chap. 5, this volume). Single deletions in the chitin
synthase genes are viable, as are chs1, chs2 and chs1,
chs3 double mutants, and only a chs2, chs3 double
deletion is lethal (Silverman et al. 1988; Shaw et al.
1991; Kollar et al. 1995; Cabib et al. 2001).
Studies with the Chs3p inhibitor nikkomycin Z
in a chs2 mutantshowedthatchitinsynthesisforthe
formation of the secondary septa is important for
survival to achieve septum closure between mother
and daughter cells (Cabib and Schmidt 2003).
The signaling cascade leading to chitin synthesis
at the septum involves the septin ring acting
as a scaffold to recruit Bni4p, which interacts
directly with Chs4p/Skt5p. Chs4p/Skt5p finally localizes
Chs3p to the septal site. Some other proteins,
namely Chs5p, Chs6p and Chs7p, are required
for the transport of Chs3p from ER or chitosome
to the plasma membrane (for reviews, see
Valdivieso et al. 1999; Munro and Gow 2001; Roncero
2002). Septa of filamentous fungi bear one
significant difference with septa of yeast-like fungi,
this being the septal pore. How this pore is gener-
Septation in Fungi 115
ated is unknown, but its presence allows the transport
of material across compartments. Using timelapse
microscopy of GFP labeled nuclei, frequent
movement of nuclei through septa was observed
(Alberti-Segui et al. 2001). Filamentous fungi need
to be able to reseal the septal pore in case of damage
to the hypha, which would otherwise cause further
damage along the hypha. This can be achieved by
clogging the septal pore with a Woronin body (Jedd
and Chua 2000; Tenney et al. 2000). The Woronin
body of N. crassa is composed of a solid core of
the Hex1 protein. Hex1 carries a peroxisomal targeting
signal, suggesting that Woronin bodies are
specialized peroxisomal structures (Jedd and Chua
2000; Tenney et al. 2000; Yuan et al. 2003). In Magnaporthe
grisea, Woronin bodies were found to
be essential for pathogenesis and growth under
nitrogen-limiting conditions (Soundararajan et al.
2004).
Since fungal cells are surrounded by a rigid
cell wall, cell growth needs to balance cell wall integrity
with cell expansion (see Sietsma and Wessels,
Chap. 4, this volume). Therefore, the activity of
chitin synthases may be counterbalanced by chitindegrading
enzymes, the chitinases. The S. cerevisiaechitinase
Cts1p is required for cell separation
of mother and daughter cells at the end of cytokinesis.
This activity is asymmetric, as the mother
retains most of its chitin ring (cf. a bud scar that can
be stained by calcofluor), whereas the daughter cell
contains a much fainter birth scar. This asymmetry
is brought about by daughter cell-specific regulatory
programs in which the transcriptional activator
of CTS1, Ace2p, is specifically localized to the
daughter cell nucleus by a signaling network that
has been termed RAM (cf. regulation of Ace2p activity
and cellular morphogenesis; Colman-Lerner
et al. 2001; Nelson et al. 2003). Filamentous fungi,
on the other hand, may not require such a chitinase
activity, since septation results only in the compartmentalization
but not in the separation of hyphal
segments. In fact, the genome of the filamentous
fungus A. gossypii does not contain a CTS1 homolog
that we recorded during our studies on the
A. gossypii WASP homolog (Walther and Wendland
2004).
Chitin synthase and chitinase activities may
counterbalance each other to ensure polarized
growth and to maintain cell wall integrity. However,
specific developmental regulation of chitin
synthases in A. nidulans, aswellastheabsence
of chitinase activity (lack of CTS1) inA. gossypii
suggest that this may not be necessary. A detailed