Abstract
AbstractThe genusAspergillusincludes industrially, medically and agriculturally important species. All of them, as do fungi in general, disperse to new niches principally by means of asexual spores. Regarding the genetic/molecular control of asexual development,Aspergillus nidulansis the main reference. In this species, two pathways control the production of conidiophores, the structures bearing asexual spores (conidia). The Upstream Developmental Activation (UDA) pathway transduces environmental signals, determining whether the Central Developmental Pathway (CDP) and the required morphological changes are induced. The transcriptional regulator BrlA links both pathways as loss-of-function mutations inflb(UDA) genes blockbrlAtranscription and, consequently, conidiation. However, the aconidial phenotype of specificflbmutants is reverted under salt-stress conditions. Previously, we generated a collection of ΔflbBmutants unable to conidiate on culture medium supplemented with NaH2PO4(0.65M). Here, we identified a Gly347Stop mutation withinflpAas responsible for the FLIP57 phenotype. The putative cyclin FlpA and the remaining putative components of the C-terminal domain kinase-1 (CTDK-1) complex are necessary for proper germination, growth and developmental patterns in bothA. nidulansandA. fumigatus. Cellular localization and functional interdependencies of the three proteins are also analyzed. Overall, this work links the putative CTDK-1 complex of aspergilli with growth and developmental control.One-sentence summaryIdentification of a mutation inflpAas inhibitor of conidiation inA. nidulansand functional characterization of FlpA, Stk47 and FlpB as putative members of the C-terminal domain kinase complex CTDK-1 in the genusAspergillus.
Publisher
Cold Spring Harbor Laboratory