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Chapter 35 : Regulation of Aspergillus Conidiation
Category: Microbial Genetics and Molecular Biology; Fungi and Fungal Pathogenesis
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This chapter discusses our current understanding of how conidiation in Aspergillus is regulated, with emphasis on the model fungus A. nidulans. The three genes (brlA, abaA, and wetA) have been proposed to define a central regulatory pathway that acts in concert with other genes to control conidiation-specific gene expression and determine the order of gene activation during conidiophore development and spore maturation. Identification and characterization of the developmental activators greatly enhanced our understanding of the molecular mechanisms for upstream regulation of conidiation in Aspergillus. Mutational inactivation of flbB, flbC, flbD, or flbE results in a third, distinct class of developmental defects classified as delayed conidiation. Importantly, while mutational inactivation of any one of these G protein components restores conidiation of the ΔflbA mutant to a certain level, no mutation can bypass the need for FluG during conidiation. Although asexual sporulation is the most common reproductive mode of many filamentous fungi, little is known about the regulatory mechanisms controlling this process. VosA plays two principal roles: (i) coupling sporogenesis and trehalose biogenesis to complete spore maturation and (ii) exerting negative-feedback regulation of developmental specific genes by repressing the expression of brlA encoding the key activator of conidiation in Aspergillus. VosA and related velvet proteins are found to be crucial global regulators for fungal development and metabolism.
Conidiophore formation and spore maturation. (A) A simplified diagram of a conidiophore (reproduced from Ni and Yu, 2007 , with permission). (B) The stages of conidiophore development in A. nidulans (adapted and modified from Mah and Yu, 2006 ). (C) The stages of conidium maturation (reproduced from Sewall et al., 1990a , with permission of the publisher). Each conidium and the phialide (P) contains a nucleus (N), mitochondria (M), endoplasmic reticulum (ER), vacuoles (V), and vesicles (Ve). Three stages (I, II, and III) of conidium maturation are shown after a conidium initial (CI) is delimited from the phialide. The phialide contains two cell wall layers: P1 and P2. The CI and conidium at stage I also contain two cell wall layers: C1 and C2. At stage II, the C2 layer condenses to form projections (*) in contact with C1. During stage III, the conidium becomes mature, containing four cell layers: C1 through C4.
Regulatory pathways of conidiation in Aspergillus nidulans. brlA→abaA→wetA constitutes the central regulatory pathway controlling conidiation. These genes cooperatively activate other genes (class A through D) responsible for the morphogenesis of conidiophores. FluG and Flb genes are upstream genes required for activation of conidiation (reviewed by Adams et al., 1998 ). The fluG repressor SfgA acts as a negative regulator of conidiation ( Seo et al., 2006 ). VosA functions as a master regulator of spore maturation, which couples sporogenesis and trehalose biogenesis to complete spore maturation and confers negative-feedback regulation of developmental specific genes by repressing the expression of brlA( Ni and Yu, 2007 ).
Central regulatory genes’ mutants and expression. (A) Phenotypes of brlA, abaA, and wetA mutants (reproduced from Boylan et al., 1987, with permission of the publisher). (B) Expression trends of central regulatory genes during conidiophore development. (C) Time and sites of expression of Aspergillus developmental genes. Data are from Boylan et al. (1987), Aguirre et al. (1990 ), Marshall and Timberlake (1991) , and Ni and Yu (2007) . The table is adapted and modified from Table 16.1 from Timberlake and Clutterbuck, 1994 .
Requirement of vosA in integrity of spores. Transmission electron microscopic analysis of 15-day-old conidiophores and 3- and 8-day-old conidia of wild-type (WT) and ΔvosA strains (adapted and modified from Ni and Yu, 2007 ). The deletion of vosA caused loss of cytoplasm and organelles including the nucleus in old conidia.
Phenotypes of fluffy mutants.
Overexpression of sfgA or vosA inhibits conidiation. (A) Overexpression of sfgA[alcA(p)::sfgA] colony exhibits white undifferentiated hyphae (fluffy) with low levels of conidiation in the center. (B) Overexpression of vosA [alcA(p)::vosA] colony exhibits complete block of conidiation (reproduced from Ni and Yu, 2007 , with permission).
The VosA/VelB/VeA/LaeA complex coordinates fungal development and mycotoxin production.
A phylogenetic tree of proteins similar to VosA (reproduced from Ni and Yu, 2007 , with permission). The ClustalV method was used for protein alignment ( Chenna et al., 2003 ), and the phylogenetic tree was generated by MegAlign in Lasergene v7.0 (DNASTAR). Abbreviations: An, A. nidulans; Af, A. fumigatus; Ao, A. oryzae; Ap, A. parasiticus; Ci, Coccidioides immitis; Mg, M. grisea; Cg, Chaetomium globosum; Nc, N. crassa; Um, Ustilago maydis; Cn, Cryptococcus neoformans; Gz, Gibberella zeae.
Models for growth and developmental control in A. nidulans and A. fumigatus(adapted and modified from Yu et al., 2006). Current models depicting upstream and downstream regulation of hyphal growth and conidiation in the two aspergilli are presented. Note that the roles of PkaA and PkaC1 in regulating conidiation are opposite.