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The gprA and gprB genes encode putative G protein‐coupled receptors required for self‐fertilization in Aspergillus nidulans
Author(s) -
Seo JeongAh,
Han KapHoon,
Yu JaeHyuk
Publication year - 2004
Publication title -
molecular microbiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.857
H-Index - 247
eISSN - 1365-2958
pISSN - 0950-382X
DOI - 10.1111/j.1365-2958.2004.04232.x
Subject(s) - aspergillus nidulans , biology , homothallism , heterothallic , gene , genetics , sexual reproduction , fungal protein , mutant , mating type
Summary The filamentous fungus Aspergillus nidulans possesses both asexual and sexual reproductive cycles. Sexual fruiting bodies (cleistothecia) can be formed in both homothallic (self) and heterothallic (outcross) conditions. In this study, we characterized two genes, gprA and gprB , that are predicted to encode putative G protein‐coupled receptors (GPCRs) similar to fungal pheromone receptors. Deletion (Δ) of gprA or gprB resulted in the production of a few small cleistothecia carrying a reduced number of ascospores, whereas Δ gprA Δ gprB eliminated fruiting body formation in homothallic conditions. However, nullifying gprA and/or gprB did not affect vegetative growth, asexual sporulation, Hülle cell formation or even cleistothecia formation in outcross, indicating that GprA and GprB are specifically required for self‐fertilization. The gprA and gprB genes encode two transcripts and, for both genes, larger transcripts are detectable during vegetative growth and asexual development whereas smaller transcripts accumulate during sexual development. Upregulation of nsdD encoding a key sexual developmental activator resulted in the production of barren cleistothecia in the Δ gprA Δ gprB mutant, suggesting that NsdD can partially rescue the developmental defects caused by deletion of GPCRs and that GprA/B‐mediated signalling may activate other genes necessary for maturation of cleistothecia and ascosporogenesis. Deletion of gprA and/or gprB suppressed growth defects caused by Δ gprD , implying that GprA/B function downstream of GprD‐mediated negative control of sexual development.