Multiple Roles of a Heterotrimeric G-Protein γ-Subunit in Governing Growth and Development of <i>Aspergillus nidulans</i>

Seo, Jeong‐Ah; Han, Kap-Hoon; Yu, Jae‐Hyuk

doi:10.1534/genetics.105.042796

Cited by 67 publications

(85 citation statements)

References 42 publications

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“…Growth signaling is primarily mediated by FadA and SfaD::GpgA (heterodimer), the a and bg subunits for a heterotrimeric G protein, respectively. When FadA (Ga) is active (GTP bound), FadA and SfaD:GpgA signal to enhance vegetative growth and repress both asexual sporulation and ST production (Yu et al 1996;Hicks et al 1997;Adams et al 1998;Rosen et al 1999;Seo et al 2005). This FadA-dependent growth-signaling pathway is in part transduced through PkaA [a catalytic subunit of cAMP-dependent protein kinase A (Shimizu and Keller 2001)].…”

Section: Discussionmentioning

confidence: 99%

NsdD Is a Key Repressor of Asexual Development inAspergillus nidulans

et al. 2014

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Asexual development (conidiation) of the filamentous fungus Aspergillus nidulans occurs via balanced activities of multiple positive and negative regulators. For instance, FluG (+) and SfgA (2) govern upstream regulation of the developmental switch, and BrlA (+) and VosA (2) control the progression and completion of conidiation. To identify negative regulators of conidiation downstream of FluG-SfgA, we carried out multicopy genetic screens using sfgA deletion strains. After visually screening .100,000 colonies, we isolated 61 transformants exhibiting reduced conidiation. Responsible genes were identified as AN3152 (nsdD), AN7507, AN2009, AN1652, AN5833, and AN9141. Importantly, nsdD, a key activator of sexual reproduction, was present in 10 independent transformants. Furthermore, deletion, overexpression, and double-mutant analyses of individual genes have led to the conclusion that, of the six genes, only nsdD functions in the FluG-activated conidiation pathway. The deletion of nsdD bypassed the need for fluG and flbA$flbE, but not brlA or abaA, in conidiation, and partially restored production of the mycotoxin sterigmatocystin (ST) in the DfluG, DflbA, and DflbB mutants, suggesting that NsdD is positioned between FLBs and BrlA in A. nidulans. Nullifying nsdD caused formation of conidiophores in liquid submerged cultures, where wild-type strains do not develop. Moreover, the removal of both nsdD and vosA resulted in even more abundant development of conidiophores in liquid submerged cultures and high-level accumulation of brlA messenger (m)RNA even at 16 hr of vegetative growth. Collectively, NsdD is a key negative regulator of conidiation and likely exerts its repressive role via downregulating brlA.T HE filamentous ascomycete Aspergillus nidulans has served as an excellent model system for studying cell biology, asexual development (conidiation), and secondary metabolism (Timberlake 1990;Martinelli 1994;Yu and Keller 2005). The A. nidulans asexual reproductive cycle can be divided into two distinct phases: growth and development. The growth phase involves germination of an asexually derived spore called a conidium and formation of an undifferentiated network of interconnected hyphal cells that form the mycelium. After a certain vegetative growth period, under appropriate conditions, some of the hyphal cells stop normal growth and begin development by forming complex structures called conidiophores that bear multiple chains of conidia (Adams et al. 1988;Park and Yu 2012a).A key and essential step for conidiophore development in Aspergillus is the activation of brlA, which encodes a C 2 H 2 zinc-finger transcription factor (TF) ( Figure 1A) (Adams et al. 1988;Chang and Timberlake 1993). Further genetic and biochemical studies identified the additional key regulators abaA and wetA that function during the middle and late stages of conidiation, respectively ( Figure 1A) (Sewall et al. 1990;Andrianopoulos and Timberlake 1991;Marshall and Timberlake 1991). These three genes have been proposed to define a c...

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Section: Discussionmentioning

confidence: 99%

NsdD Is a Key Repressor of Asexual Development inAspergillus nidulans

et al. 2014

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“…Another key role of FluG is thought to be posttranscriptional activation of FlbA (Lee and Adams 1996), which in turn attenuates vegetative proliferation signaling mediated by a heterotrimeric G protein composed of FadA (Ga), SfaD (Gb), and GpgA (Gg) Rosén et al 1999;Seo et al 2005). Constitutive activation of this FadA signaling blocks development and production of ST (see Figure 1; Yu et al 1996Yu et al , 1999Hicks et al 1997).…”

Section: Discussionmentioning

confidence: 99%

FluG-Dependent Asexual Development in Aspergillus nidulans Occurs via Derepression

Seo¹,

2006

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The asexual spore is one of the most crucial factors contributing to the fecundity and fitness of filamentous fungi. Although the developmental activator FluG was shown to be necessary for activation of asexual sporulation (conidiation) and production of the carcinogenic mycotoxin sterigmatocystin (ST) in the model filamentous fungus Aspergillus nidulans, the molecular mechanisms underlying the developmental switch have remained elusive. In this study, we report that the FluG-mediated conidiation in A. nidulans occurs via derepression. Suppressor analyses of fluG led to the identification of the sfgA gene encoding a novel protein with the Gal4-type Zn(II) 2 Cys 6 binuclear cluster DNA-binding motif at the N terminus. Deletion (D) and 31 other loss-of-function sfgA mutations bypassed the need for fluG in conidiation and production of ST. Moreover, both DsfgA and DsfgA DfluG mutations resulted in identical phenotypes in growth, conidiation, and ST production, indicating that the primary role of FluG is to remove repressive effects imposed by SfgA. In accordance with the proposed regulatory role of SfgA, overexpression of sfgA inhibited conidiation and delayed/reduced expression of conidiation-and STspecific genes. Genetic analyses demonstrated that SfgA functions downstream of FluG but upstream of transcriptional activators (FlbD, FlbC, FlbB, and BrlA) necessary for normal conidiation.

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“…Deletion of RGS2 causes prolonged activation of Gpa2-PKA and thereby increases the sensitivity of cells to thermal stress, while overexpression of RGS2 causes significant elevation in heat resistance (41). Recent studies showed that GanB (a G␣ similar to Gpa2 [4]) functions in sensing external carbon sources and controlling spore germination via a cAMP/PKA pathway in A. nidulans, where SfaD-GpgA (G␤␥) is predicted to function in activating GanB (19,30,33). Furthermore, we demonstrated that GanB signaling activates thermal and oxidative stress responses, which are negatively controlled by RgsA (an RGS protein similar to Rgs2 in yeast [13]).…”

Section: Discussionmentioning

confidence: 99%

The pkaB Gene Encoding the Secondary Protein Kinase A Catalytic Subunit Has a Synthetic Lethal Interaction with pkaA and Plays Overlapping and Opposite Roles in Aspergillus nidulans

Rierson²,

Seo³

et al. 2005

Eukaryot Cell

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Filamentous fungal genomes contain two distantly related cyclic AMP-dependent protein kinase A catalytic subunits (PKAs), but only one PKA is found to play a principal role. In Aspergillus nidulans, PkaA is the primary PKA that positively functions in vegetative growth and spore germination but negatively controls asexual sporulation and production of the mycotoxin sterigmatocystin. In this report, we present the identification and characterization of pkaB, encoding the secondary PKA in A. nidulans. Although deletion of pkaB alone does not cause any apparent phenotypic changes, the absence of both pkaB and pkaA is lethal, indicating that PkaB and PkaA are essential for viability of A. nidulans. Overexpression of pkaB enhances hyphal proliferation and rescues the growth defects caused by ⌬pkaA, indicating that PkaB plays a role in vegetative growth signaling. However, unlike ⌬pkaA, deletion of pkaB does not suppress the fluffy-autolytic phenotype resulting from ⌬flbA. While upregulation of pkaB rescues the defects of spore germination resulting from ⌬pkaA in the presence of glucose, overexpression of pkaB delays spore germination. Furthermore, upregulation of pkaB completely abolishes spore germination on medium lacking a carbon source. In addition, upregulation of pkaB enhances the level of submerged sporulation caused by ⌬pkaA and reduces hyphal tolerance to oxidative stress. In conclusion, PkaB is the secondary PKA that has a synthetic lethal interaction with PkaA, and it plays an overlapping role in vegetative growth and spore germination in the presence of glucose but an opposite role in regulating asexual sporulation, germination in the absence of a carbon source, and oxidative stress responses in A. nidulans.

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Multiple Roles of a Heterotrimeric G-Protein γ-Subunit in Governing Growth and Development of Aspergillus nidulans

Cited by 67 publications

References 42 publications

NsdD Is a Key Repressor of Asexual Development inAspergillus nidulans

NsdD Is a Key Repressor of Asexual Development inAspergillus nidulans

FluG-Dependent Asexual Development in Aspergillus nidulans Occurs via Derepression

The pkaB Gene Encoding the Secondary Protein Kinase A Catalytic Subunit Has a Synthetic Lethal Interaction with pkaA and Plays Overlapping and Opposite Roles in Aspergillus nidulans

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