Growth, Differentiation and Sexuality

stimulated Neurospora colonial growth and hyphal
branching, and inhibited the effect of light on cot-1
transcription (Lauter et al. 1998). However, the
amount of COT-1 protein in the cell, as measured
by specific antibodies, was not altered by light
(Gorovits et al. 1999), a puzzling observation that
suggested that the role of the short cot-1 transcript
and the effect of light on cot-1 transcription
and hyphal branching remain to be elucidated.
Another, yet again puzzling, role for COT-1 has
been proposed, based on the fact that a cot-1
mutation suppressed the blind phenotype of a
wc-2 strain. Strains carrying a mutation in the
gene wc-2 and a temperature-sensitive mutation
in cot-1 showed a normal photoactivation of
the clock-controlled gene ccg-1 only when the
experiments were carried out at the permissive
temperature. This suppression of the wc-2 phenotype
was very specific, since the wc-2 cot-1 strain
did not show photoactivation of al-3 or ccg-2, and
the cot-1 mutation did not suppress the blindness
of a wc-1 mutant (Arpaia et al. 1995). The results
showed that a partially active COT-1 kinase might
bypass the effect of the wc-2 mutation for the
photoactivation of some Neurospora genes (Arpaia
et al. 1995).
c) Photoconidiation
Conidiation in Neurospora is a developmental process
that is induced by several environmental cues
such as desiccation, lack of nitrogen or carbon,
and the presence of light (reviewed by Springer
1993; see Chap. 14, this volume). Light is required
to obtain the maximum number of conidia, but it
produces only a modest fourfold increment in the
amount of conidia over that obtained in cultures
kept in the dark (Lauter et al. 1997). Interestingly,
the photoactivation of conidiation is 500-fold in
a strain with a thermosensitive mutation in the
gene acon-2. This strain conidiates only at the permissive
temperature, 25 ◦C, but the mycelium remains
undifferentiated when it is grown at 34 ◦C. At the permissive temperature, the number of conidia
developed by the acon-2 strain is very low but
it reaches the amount produced by the wild type
upon exposure to light (Lauter et al. 1997). It seems
that a partially functional ACON2 protein represses
conidiation in the dark, allowing light-dependent
conidiation to be fully observed.
Other proteins and chemicals may play a role
in Neurospora photoconidiation. A role for the
flavoprotein nitrate reductase in Neurospora pho-
Photomorphogenesis and Gravitropism 237
toconidiation has been suggested, based on the lack
of light-induced conidiation in mutants without
detectable nitrate reductase activity (Ninnemann
1991). Additionally, a role for nitric oxide synthase
and nitric oxide in Neurospora conidiation and its
regulation by light has been proposed based on the
effect of inhibitors of the enzyme and nitric oxide
donors on photoconidiation (Ninnemann and
Maier 1996). The photoinduction of conidiation,
like all the Neurospora photoresponses, requires
the wc gene products (Lauter et al. 1997), but an
earlier report showed that conidiation of a wc-1
mutant was promoted by light (Ninnemann 1991).
The different nitrogen sources used in the growth
medium may be responsible for the different
photoconidation phenotype of the wc-1 mutant
(Lauter et al. 1997). These results suggest a complex
interaction of nutritional and environmental
factors in the regulation of Neurospora conidiation.
Conidiation in Neurospora is also governed by
a circadian clock that can be entrained by a light
exposure. The interested reader should consult the
chapter on the Neurospora circadian clock by Dunlap
et al. (2004) in this series (The Mycota, Vol. 3,
2nd edn.), and other reviews on this topic by Bell-
Pedersen (2000), Merrow et al. (2001b), Liu (2003),
Crosthwaite (2004), Dunlap and Loros (2004), and
Lakin-Thomas and Brody (2004).
The development of conidiophores and conidia
should bring about differential gene expression
that could be modulated by blue light. Indeed,
some genes in Neurospora are induced by
conidiation and blue light (Lauter and Russo 1991;
Lauter et al. 1992; Lauter and Yanofsky 1993; Carattoli
et al. 1995), and their promoters have an array
of developmental-, light-, and circadian clockcontrolled
DNA elements (Corrochano et al. 1995;
Bell-Pedersen et al. 1996; Lee and Ebbole 1998).
Mutants altered in the regulation of light-induced
geneshavebeenisolated,somehavingdefectsinthe
regulation of conidiation (Madi et al. 1994; Carattoli
et al. 1995; Linden et al. 1997b). The genes altered
in two mutants have been cloned and identified as
a general repressor of gene expression (Yamashiro
et al. 1996) and a glucose transporter (Madi et al.
1997), which confirmed the complex relationship
between light, nutrient deprivation, and conidiation
in Neurospora. The regulation of gene expression
by light and development are likely to be
primary events in the induction of conidiation by
light, and are a promising avenue of research to
unravel the molecular mechanism of Neurospora
photomorphogenesis.