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72 CHAPTER 4

are continually added at the extreme tip (Fig. 4.6).
Then the wall rigidifies progressively by the formation
of extra bonds behind the tip. This is reminiscent
of Robertson’s original idea of a plastic, deformable
wall at the extreme tip, with subsequent rigidification
occurring behind the tip. Thus, for example, if the
supply of vesicles to the tip is slowed or halted (by
an osmotic shock, etc.) the rate of hyphal extension
would slow or stop, but wall cross-linking might be
unaffected if bonding occurs spontaneously within the
wall. We could therefore have at least some of the ele-
ments of a unifying theory of fungal tip growth, based
on much biochemical and ultrastructural evidence. It
is still necessary to explain how hyphae with an essen-
tially fluid (viscoelastic) wall could resist turgor pres-
sure, but the answer to this could lie in the structural
support provided by the massive actin cytoskeleton at
the hyphal tip, as we saw in Chapter 3.
Jackson & Heath (1990) investigated this for
Saprolegnia ferax (Oomycota). They showed that treat-
ment of hyphae with cytochalasin E (one of several
cytochalasins, which disrupt cell dynamics by binding
to actin microfilaments) caused disruption of the actin
cap and led initially to an increase in the rate of tip
extension, but then the tips swelled and burst. The weak-
est region of the tip, most susceptible to bursting, was
not the extreme apex where the actin cap is densest
but on the shoulders of the apex where the actin is less
dense and where the wall presumably has not yet
rigidified sufficiently to compensate for the weaker
cytoskeleton. It will be recalled that the shoulder of the
apex is where new tips originate when hyphae are
flooded with water (Fig. 4.3).
Another important aspect of the steady-state model
is that it could help to explain how fungi release
enzymes into the environment for breakdown of com-
plex polymers. As explained in Chapter 6, enzymes
are relatively large molecules, commonly in the range
of 30–50 kDa (kiloDaltons), and there is no evidence
that fungal walls have continuous pores of this size
through which enzymes could be released into the
environment. The viscoelastic wall model could help

to resolve this problem if the enzymes are released from

vesicles that fuse with the hyphal tip and these enzymes

then flow outwards through the developing wall.

The driving force for apical growth

Having considered the dynamics of wall growth and

wall rigidification, the remaining question concerns the

driving force for apical extension. The cytoskeletal

components have emerged as the strongest candidates

for this, consistent with many studies on animal cells

where protrusions such as pseudopodia are linked to

the polymerization of actin.

Studies on Saprolegnia (Oomycota) have shown

that the apex can extend even when hyphae have

negligible turgor pressure, presumably because actin

polymerization drives this process (reviewed by Money

1995). Actin is abundant in hyphal tips, and both

tip extension and cytoplasmic streaming can be halted

by treating fungi with cytochalasins (“cell-relaxers”)

which bind to actin. In S. cerevisiaethere is strong

evidence that F-actin is involved in the localization of

bud formation and that it interacts with the motor pro-

tein myosin to transport vesicles to the bud site.

The question of whether microtubules are directly

involved in fungal tip growth is more problematical.

Hyphal extension can be halted by the benzimidazole

fungicides, the related azole drugs, and griseofulvin (see

Chapter 17), all of which interfere with microtubule

function. Coinciding with this stoppage of growth, there

is a progressive depletion of vesicles in the hyphal tip

(Howard & Aist 1980). Thus, microtubules must in some

way be involved in tip growth – perhaps by providing

tramlines for vesicle cargoes. Calcium also seems to be

intimately involved in tip growth (Jackson & Heath

1993) because the tips of several fungi, including

Neurospora, and also Saprolegnia(Oomycota), require

external calcium for continued tip growth. Moreover,

the plasmalemma at the extreme tip is reported to have

a high concentration of stretch-activated calcium

channels, allowing the ingress of calcium when the

Fig. 4.6Representation of the steady-state

model of hyphal tip growth, in which the

wall is envisaged as being viscoelastic. New wall

polymers synthesized at the extreme tip are

suggested to flow outwards and backwards

as new components are continually added at

the tip. The decreasing thickness of the arrows

behind the tip signifies progressively reduced

flow as the polymers become cross-linked.

(Based on a diagram in Wessels 1990.)