J. Wieser et Th. Adams, FLBD ENCODES A MYB-LIKE DNA-BINDING PROTEIN THAT COORDINATES INITIATION OF ASPERGILLUS-NIDULANS CONIDIOPHORE DEVELOPMENT, Genes & development, 9(4), 1995, pp. 491-502
The timing of asexual fruiting body formation during Aspergillus nidul
ans colony development is precisely regulated so that conidiophores ar
e typically produced 1-2 mm behind the growing edge of the colony. Mut
ations in any of four A. nidulans genes, flbB, flbC, flbD, or flbE, re
sult in colonies that are delayed at least 24 hr in their ability to i
nitiate conidiophore development resulting in fluffy colonies with con
idiophores forming in the center, at least 12-15 mm behind the growing
edge. The requirement for each of these four genes in determining the
timing of developmental initiation precedes transcriptional activatio
n of the primary developmental regulatory gene brlA, indicating a poss
ible role for each gene in developmentally regulated activation of brl
A expression. The wild-type flbD gene was isolated and shown to encode
an similar to 1.6-kb mRNA that is present throughout the A. nidulans
life cycle. The deduced FlbD protein sequence predicts a 314-amino-aci
d polypeptide with significant identity at its amino terminus to the D
NA-binding domain of the Myb family of transcription factors indicatin
g that FlbD probably functions as a sequence-specific transcriptional
activator. Although conidiophore development does not normally occur i
n submerged culture, forced overexpression of flbD in submerged hyphae
caused inappropriate activation of brlA expression and resulted in pr
oduction of complex conidiophores that produced all of the distinct ce
ll types observed in wild-type conidiophores including viable spores.
This ability of flbD overexpression to activate conidiation requires b
rlA, flbB, and flbA (another early developmental regulator) but does n
ot require flbC or flbE. We propose that FlbD functions during normal
development by activating transcription of other genes required for de
velopment (such as brlA) and that FlbD activity is normally controlled
post-transcriptionally by an unknown mechanism.