Growth, Differentiation and Sexuality

240 L.M. Corrochano and P. Galland
red light is effective, and the stimulatory effect may
bereversediffar-redlightisappliedafterared-light
exposure, suggesting a phytochrome-like photoreceptor
in Aspergillus, like those involved in plant
photobiology (Mooney and Yager 1990). The similarity
of the amino-end of the Aspergillus BRLA
protein, a master regulator of conidiation, with the
segment involved in light-induced conformational
changes of several plant phytochromes has fuelled
the idea that a phytochrome-like photoreceptor
may directly regulate conidiation in Aspergillus
(Griffith et al. 1994). The recent discovery of a phytochrome
gene in the Aspergillus nidulans genome
could give important clues to the nature of the photoreceptor
involved in red-light conidiation (Blumenstein
et al. 2005).
Amutationinthevelvet (veA)geneallowsAspergillus
to conidiate in the dark, suggesting a role
for the veA gene product as a negative regulator
of light-induced conidiation (Mooney and Yager
1990). The veA1 mutant has suffered a nucleotide
change in the initiation codon, resulting in a 36amino
acid shorter protein due to the presumed
initiation in a secondary methionine codon (Kim
et al. 2002). RNA expression and gene overexpression
experiments have suggested that the veA gene
product is also a positive activator of sexual development
(Kim et al. 2002; see Chap. 16, this volume).
Ahomologofvelvet has been identified in the Neurospora
genome, suggesting that it may play a similar
role for Neurospora photoconidiation (Galagan
et al. 2003). Suppressors of the veA1 mutations
that restored a light-dependent conidiation have
been isolated (Mooney et al. 1990), and three of
these are alleles of the fluG gene (Yager et al. 1998),
a gene previously identified by mutations resulting
in a conidial and fluffy phenotype. Additionally,
a mutant strain of Aspergillus that conidiates
under red or blue light has been used to isolate
a mutant that blocks red light-induced conidiation.
Interestingly, the mutant altered in red-light conidiation
is yet another allele of the fluG gene (Yager
et al. 1998). FLUG is a protein with limited similarity
with prokaryotic glutamine synthetases, and
is involved in the synthesis of a diffusible, lowmolecular
weight factor that controls the initiation
of sporulation (Lee and Adams 1994; see Chap. 11,
this volume). The isolation of fluG alleles that modified
light-dependent conidiation in Aspergillus suggested
an important role for FLUG in the regulation
of conidiation by light (Yager et al. 1998). In
addition to VEA and FLUG, a role for the COP9
signalosome in light regulation of Aspergillus de-
velopment has been suggested (Busch et al. 2003).
A csnD deletion strain is missing one of the components
of COP9 and is blind for light regulation
of development, since it produced sexual development
in plates grown in light or dark. The results
suggest that in Aspergillus the COP9 signalosome,
which is involved in targeting proteins for degradation,
is essential for light-dependent signaling
(Busch et al. 2003).
b) Effect of Light on Sexual Development
and the Circadian Rhythm
Sexual development in Aspergillus is inhibited by
red light, and is also affected by the presence of
fatty acids added to the culture media or modified
in the cell by mutations (Calvo et al. 1999, 2001; see
Chap. 16, this volume). The Aspergillus nidulans
genome contains a gene, phsA, for a protein very
similar to a bacterial phytochrome. The Aspergillus
phytochromeactsasared-lightsensorandcould
be a photoreceptor for the red-light inhibition of
sexual development (Blumenstein et al. 2005).
Circadian rhythms have also been described in
Aspergillus.InAspergillus flavus,thedevelopment
of one type of survival structures, sclerotia, is governed
by a circadian clock with a period of 33 h
at 30 ◦C (Greene et al. 2003). However, no circadian
rhythm in the development of morphological
structures could be observed in Aspergillus nidulans,
but the transcription of the glyceraldehyde-
3-phosphate dehydrogenase gene (gpdA) followed
arhythmthatcouldbeentrainedbylightandtemperature,
suggesting the presence of a circadian
clock (Greene et al. 2003). The lack of an obvious
circadian rhythm in Aspergillus development
is not surprising, since the Neurospora circadian
clock for conidia formation, now a model for circadian
regulation, was fully uncovered after the isolationofastraincarryingaband
mutation (Dunlap
et al. 2004). It is thus conceivable that, similarly
to Neurospora, a mutant strain of Aspergillus
could be isolated showing some sort of morphological
circadian clock. The Aspergillus genome lacks
a homolog of the Neurospora frq gene, a key element
in the Neurospora circadian clock, but containshomologsofthewc
genes that are required
for Neurospora blue-light photoresponses and that
play important roles in the proper regulation of the
circadian clock (Greene et al. 2003). These observations
suggest that the Aspergillus circadian clock
may be organized using some, but not all, of the
elements of the Neurospora clock.