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  • American Society for Microbiology  (3)
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  • American Society for Microbiology  (3)
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  • 1
    Online Resource
    Online Resource
    Differential Roles of the ChiB Chitinase in Autolysis and Cell Death of Aspergillus nidulans
    American Society for Microbiology ; 2009
    In:  Eukaryotic Cell Vol. 8, No. 5 ( 2009-05), p. 738-746
    Details
    In: Eukaryotic Cell, American Society for Microbiology, Vol. 8, No. 5 ( 2009-05), p. 738-746
    Abstract: Autolysis is a natural event that occurs in most filamentous fungi. Such self-degradation of fungal cells becomes a predominant phenomenon in the absence of the regulator of G protein signaling FlbA in Aspergillus nidulans . Among a number of potential hydrolytic enzymes in the A. nidulans genome, the secreted endochitinase ChiB was shown to play a major role in autolysis. In this report, we investigate the roles of ChiB in fungal autolysis and cell death processes through genetic, biochemical, and cellular analyses using a set of critical mutants. Determination of mycelial mass revealed that, while the flbA deletion (Δ flbA ) mutant autolyzed completely after a 3-day incubation, the Δ flbA Δ chiB double mutant escaped from hyphal disintegration. These results indicate that ChiB is necessary for the Δ flbA -induced autolysis. However, importantly, both Δ flbA and Δ flbA Δ chiB strains displayed dramatically reduced cell viability compared to the wild type. These imply that ChiB is dispensable for cell death and that autolysis and cell death are separate processes. Liquid chromatography-tandem mass spectrometry analyses of the proteins that accumulate at high levels in the Δ flbA and Δ flbA Δ chiB mutants identify chitinase (ChiB), dipeptidyl peptidase V (DppV), O -glycosyl compound hydrolase, β- N -acetylhexosaminidase (NagA), and myo -inositol-1-phosphate synthase (InoB). Functional characterization of these four genes reveals that the deletion of nagA results in reduced cell death. A working model bridging G protein signaling and players in autolysis/cell death is proposed.
    Type of Medium: Online Resource
    ISSN: 1535-9778 , 1535-9786
    URL: Article
    DOI: 10.1128/EC.00368-08
    Language: English
    Publisher: American Society for Microbiology
    Publication Date: 2009
    detail.hit.zdb_id: 2071564-X
    SSG: 12
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  • 2
    Online Resource
    Online Resource
    The Putative Guanine Nucleotide Exchange Factor RicA Mediates Upstream Signaling for Growth and Development in Aspergillus
    American Society for Microbiology ; 2012
    In:  Eukaryotic Cell Vol. 11, No. 11 ( 2012-11), p. 1399-1412
    Details
    In: Eukaryotic Cell, American Society for Microbiology, Vol. 11, No. 11 ( 2012-11), p. 1399-1412
    Abstract: Heterotrimeric G proteins (G proteins) govern growth, development, and secondary metabolism in various fungi. Here, we characterized ricA , which encodes a putative GDP/GTP exchange factor for G proteins in the model fungus Aspergillus nidulans and the opportunistic human pathogen Aspergillus fumigatus . In both species, ricA mRNA accumulates during vegetative growth and early developmental phases, but it is not present in spores. The deletion of ricA results in severely impaired colony growth and the total (for A. nidulans ) or near (for A. fumigatus ) absence of asexual sporulation (conidiation). The overexpression (OE) of the A. fumigatus ricA gene (Af ricA ) restores growth and conidiation in the ΔAn ricA mutant to some extent, indicating partial conservation of RicA function in Aspergillus . A series of double mutant analyses revealed that the removal of RgsA (an RGS protein of the GanB Gα subunit), but not sfgA , flbA , rgsB , or rgsC , restored vegetative growth and conidiation in ΔAn ricA . Furthermore, we found that RicA can physically interact with GanB in yeast and in vitro . Moreover, the presence of two copies or OE of pkaA suppresses the profound defects caused by ΔAn ricA , indicating that RicA-mediated growth and developmental signaling is primarily through GanB and PkaA in A. nidulans . Despite the lack of conidiation, brlA and vosA mRNAs accumulated to normal levels in the Δ ricA mutant. In addition, mutants overexpressing fluG or brlA (OE fluG or OE brlA ) failed to restore development in the ΔAn ricA mutant. These findings suggest that the commencement of asexual development requires unknown RicA-mediated signaling input in A. nidulans .
    Type of Medium: Online Resource
    ISSN: 1535-9778 , 1535-9786
    URL: Article
    DOI: 10.1128/EC.00255-12
    Language: English
    Publisher: American Society for Microbiology
    Publication Date: 2012
    detail.hit.zdb_id: 2071564-X
    SSG: 12
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  • 3
    Online Resource
    Online Resource
    Basic-Zipper-Type Transcription Factor FlbB Controls Asexual Development in Aspergillus nidulans
    American Society for Microbiology ; 2008
    In:  Eukaryotic Cell Vol. 7, No. 1 ( 2008-01), p. 38-48
    Details
    In: Eukaryotic Cell, American Society for Microbiology, Vol. 7, No. 1 ( 2008-01), p. 38-48
    Abstract: The fungal colony is a complex multicellular unit consisting of various cell types and functions. Asexual spore formation (conidiation) is integrated through sensory and regulatory elements into the general morphogenetic plan, in which the activation of the transcription factor BrlA is the first determining step. A number of early regulatory elements acting upstream of BrlA ( fluG and flbA-E ) have been identified, but their functional relations remain to be further investigated. In this report we describe FlbB as a putative basic-zipper-type transcription factor restricted to filamentous fungi. FlbB accumulates at the hyphal apex during early vegetative growth but is later found in apical nuclei, suggesting that an activating modification triggers nuclear import. Moreover, proper temporal and quantitative expression of FlbB is a prerequisite for brlA transcription, and misscheduled overexpression inhibits conidiation. We also present evidence that FlbB activation results in the production of a second diffusible signal, acting downstream from the FluG factor, to induce conidiation.
    Type of Medium: Online Resource
    ISSN: 1535-9778 , 1535-9786
    URL: Article
    DOI: 10.1128/EC.00207-07
    Language: English
    Publisher: American Society for Microbiology
    Publication Date: 2008
    detail.hit.zdb_id: 2071564-X
    SSG: 12
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