flbD encodes a Myb-like DNA-binding protein that coordinates initiation of Aspergillus nidulans conidiophore development.

Abstract

The timing of asexual fruiting body formation during Aspergillus nidulans colony development is precisely regulated so that conidiophores are typically produced 1-2 mm behind the growing edge of the colony. [Key Words: flbD; myb; conidiation; fungi; brlA; microbial development] Received December 7, 1994; revised version accepted January 20, 1995. Asexual reproduction in the filamentous fungus Aspergillus nidulans is a continual progression that begins with newly forming hyphae at the growing edge of the colony and progresses through differentiation of specialized cells 1-2 mm behind the leading edge of the mycelium and gives rise to multicellular spore-bearing structures, termed conidiophores (Navarro-Bordonaba and Adams 1994). The initiation of A. nidulans conidiophore development, in contrast to initiation of sporulation in many other microorganisms, is not normally triggered by unfavorable environmental conditions but instead occurs as a precisely timed, genetically programmed event in the life cycle in response to internal and external cues (Pastushok and Axelrod 1976;Champe et al. 1981;Adams et al. 1992). The molecular genetic events regulating onset of conidiation are not fully understood but ultimately result in the controlled activation of a transcriptional cascade leading to the expression of hundreds of essential (Clutterbuck 1969; Martinelli and Clutterbuck 1971;Stringer et al. 1991) and nonessential genes (Aramayo et al. 1989). Several lines of evidence indicate that a primary activator of sporulation-specific gene expression is BrlA, a C2H2 zinc finger nucleic acid-binding protein (Adams et al. 1988(Adams et al. , 1990Chang and Timberlake 1992). brlA mRNA is present at extremely low levels in hyphae and begins to accumulate shortly after developmental induction (Boylan et al. 1987;Han et al. 1993;Prade and Timberlake 1993). brlA is required for activation of other sporulation-specific genes including at least two developmental regulatory genes, abaA and wetA while brlA null mutants produce abnormal developmental structures that initially resemble conidiophore stalks but grow indeterminately, failing to differentiate other specialized cell types (Clutterbuck 1969;Boylan et al. 1987). The pivotal role for brlA in controlling activation of the conidiation pathway is most strongly supported by the observation that forced activation of brlA in vegetative hyphae re- expression (Wieser et al. 1994). Mutations in any one of these genes result in colonies that fail to make the programmed switch from undifferentiated vegetative hyphal growth at the edge of the colony to conidiophore development within. These mutants have diverse phenotypes, but all produce large masses of undifferentiated aerial hyphae that give the colony a "fluffy" or cottonlike appearance. Fluffy mutants resulting from loss of fluG function can be distinguished from strains with mutations in any of the other five genes in at least two ways. First, although fluG mutants are unable to activate brlA expression normally, the requirement...

KapI, a non-essential member of the Pse1p/Imp5 karyopherin family, controls colonial and asexual development in Aspergillus nidulans

“…The results obtained in this work lead us to propose that KapI is not the importer of FlbB. In addition, as brlA is expressed in the null DkapI background but not in flbD null (Wieser & Adams, 1995) or flbC mutants (Wieser et al, 1994), we discard the possibility of an exclusive import of those two TFs by KapI.…”

“…Mutations in most UDA genes generate a phenotype commonly known as 'fluffy', which shows delayed or impaired conidiation (Etxebeste et al, 2009, and references therein). Many UDAs are putative TFs (Adams et al, 1998;Etxebeste et al, 2008;Seo et al, 2006;Wieser & Adams, 1995). The best-known member of this family is the bZIPtype TF FlbB, which is localized in the most apical nucleus of vegetative hyphae, and remarkably, in the Spitzenkörper (Etxebeste et al, 2008Garzia et al, 2009).…”

FluG-Dependent Asexual Development in Aspergillus nidulans Occurs via Derepression

“…Mutations in any of these genes result in ''fluffy'' colonies that are characterized by undifferentiated cotton-like masses of vegetative cells (reviewed in Adams et al 1998). The possible genetic interactions between various flb genes were examined and the two genetic regulatory cascades have been proposed (Figure 1), in which the fluG gene functions most upstream (Wieser and Adams 1995;Lee and Adams 1996).…”

“…Briefly, the alcA promoter (Gwynne et al 1987) and the sfgA ORF with terminator were amplified using the primer pairs OJA106-107 and OYG11-28, respectively, and fused as described . The alcA(p)TsfgA fusion product was amplified with OJA108 and OYG29, and the final amplicon was digested with BamHI and ligated into the BamHI cut pSH96 plasmid (Wieser and Adams 1995). The sequence verified that the alcA(p)TsfgA plasmid was introduced into FGSC237 (Table 1).…”

NsdD Is a Key Repressor of Asexual Development inAspergillus nidulans

“…FlbD (a cMyb-type TF) and FlbB then cooperatively function in activating expression of brlA (Garzia et al 2010). Both of these two independent conidiation activation cascades ( Figure 1A) are necessary for full activation of brlA expression and proper conidiation (Wieser and Adams 1995;Garzia et al 2010;Kwon et al 2010a). Importantly, loss of fluG or flbA function results in the blockage in both conidiation and production of the carcinogenic mycotoxin sterigmatocystin (ST), the penultimate precursor of the betterknown potent carcinogen aflatoxins (Lee and Adams 1994a;Hicks et al 1997).…”