A putative G protein-coupled receptor controls growth, germination and coordinated development in Aspergillus nidulans.

Kap-Hoon Han, Jeong-Ah Seo and Jaehyuk Yu.

Abstract: 

Comprehensive comparative genomic studies on heterotrimeric G-protein signal transduction components lead us to identify seven genes (gprA~gprG) that are predicted to encode putative seven-transmembrane spanning G protein-coupled receptors (GPCRs) in Aspergillus nidulans. Functional characterization of four (gprA~gprD) GPCRs has been carried out and disruption of gprD resulted in extreme phenotypic abnormalities. The gprD gene is predicted to encode a 427 amino acid polypeptide with typical seven transmembrane domains. The gprD null mutant exhibits severely reduced colony growth and highly elevated fruiting body formation, implying that the mutant fails to coordinate balanced growth and development. Moreover, the timing of spore germination of thegprD null mutant is delayed at least two hours, indicating GprD may also play a crucial role in germination. In order to examine whether extreme growth reduction is caused by uncontrolled activation of sexual development, double mutants of gprD deletion and deletion of the genes related to sexual differentiation were generated. Both double deletion mutants of gprD; nsdD and gprD; veA showed no fruiting body formation and restored hyphal growth to near wild-type level. Furthermore, environmental conditions, including poor carbon source and/or high levels of salt, that induce asexual development and block sexual development also caused the recovered growth with the absence of fruiting body in the gprD null mutant. These results clearly suggest that the primary role of GprD is to repress and coordinate sexual development and to confer proper growth during the lifecycle. Further studies to dissect genetic components functioning downstream of GprD are in progress.
2003

abstract No: 

Fungal Genet. Newsl. 50 (Supl):abstract

Full conference title: 

22nd Fungal Genetics Conference
    • Fungal Genetics Conference 22nd (2001)