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Eukaryotic Cell, February 2006, p. 400-410, Vol. 5, No. 2
1535-9778/06/$08.00+0     doi:10.1128/EC.5.2.400-410.2006
Copyright © 2006, American Society for Microbiology. All Rights Reserved.

The Phosducin-Like Protein PhnA Is Required for Gß-Mediated Signaling for Vegetative Growth, Developmental Control, and Toxin Biosynthesis in Aspergillus nidulans

Department of Food Microbiology and Toxicology, Food Research Institute,¹ Molecular & Environmental Toxicology Center, University of Wisconsin, Madison, Wisconsin 53706²

Received 21 October 2005/ Accepted 16 November 2005

Phosducin or phosducin-like protein (PhLP) is a positive regulator of Gß activity. The Gß (SfaD) and G (GpgA) subunits function in vegetative growth and developmental control in the model filamentous fungus Aspergillus nidulans. To better understand the nature of Gß-mediated signaling, phnA, encoding an A. nidulans PhLP, has been studied. Deletion of phnA resulted in phenotypes almost identical to those caused by deletion of sfaD, i.e., reduced biomass, asexual sporulation in liquid submerged culture, and defective fruiting body formation, suggesting that PhnA is necessary for Gß function. The requirement for the RGS protein FlbA in asexual sporulation could be bypassed by the phnA mutation, indicating that PhnA functions in FlbA-controlled vegetative growth signaling, primarily mediated by the heterotrimeric G protein composed of FadA (G), SfaD, and GpgA. However, whereas deletion of fadA restored both asexual sporulation and the production of sterigmatocystin (ST), deletion of sfaD, gpgA, or phnA failed to restore ST production in the flbA mutant. Further studies revealed that SfaD, GpgA, and PhnA are necessary for the expression of aflR, encoding the transcriptional activator for the ST biosynthetic genes, and subsequent ST biosynthesis. Overexpression of aflR bypassed the need for SfaD in ST production, indicating that the results of SfaD-mediated signaling may include transcriptional activation of aflR. Potential differential roles of FadA, Gß, and FlbA in controlling ST biosynthesis are further discussed.

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