Regulation of Fungal Morphogenesis and Gene Expression

A special issue of Journal of Fungi (ISSN 2309-608X).

Deadline for manuscript submissions: closed (30 November 2018)

Special Issue Editor


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Guest Editor
Geisel School of Medicine at Dartmouth, Microbiology, and Molecular Pathogenesis Program, Hanover, NH, USA
Interests: molecular mechanisms of fungal pathogenesis; candida albicans / generating stratagies for improved prevention and therapy for fungal infections

Special Issue Information

Dear Colleagues,

Many fungi adapt to dynamic environmental conditions by changing their cellular growth patterns while simultaneously altering gene expression. For fungal pathogens, morphogenesis and gene expression changes are critical for invasion of host tissue and disease. Understanding the fundamental mechanisms that ensure appropriate gene expression patterns and levels during and following morphogenesis could open up new avenues for interfering with the pathogenic properties of fungi. While progress has been made in identifying the proteins that carry out changes in cell growth patterns during morphogenesis and the transcription factors that regulate gene expression changes, little is known about how these processes are coordinated. More research is needed to determine if there is crosstalk between the morphogenesis machinery and transcription factors, or if these two processes respond to environmental conditions independently. To help address this question, papers are sought that will highlight research that elucidates mechanisms that regulate fungal morphogenesis, morphology-specific gene expression, and the connections between these two processes.

Sincerely,

Dr. Paula R. Sundstrom
Guest Editor

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Keywords

  • fungal cellular growth
  • fungal gene expression
  • fungal morphogenesis
  • fungal hyphae
  • transcription factors

Published Papers (4 papers)

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Research

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21 pages, 3909 KiB  
Article
Deletion of ptn1, a PTEN/TEP1 Orthologue, in Ustilago maydis Reduces Pathogenicity and Teliospore Development
by Lalu M. K. Vijayakrishnapillai, John S. Desmarais, Michael N. Groeschen and Michael H. Perlin
J. Fungi 2019, 5(1), 1; https://doi.org/10.3390/jof5010001 - 20 Dec 2018
Cited by 8 | Viewed by 3734
Abstract
The PTEN/PI3K/mTOR signal transduction pathway is involved in the regulation of biological processes such as metabolism, cell growth, cell proliferation, and apoptosis. This pathway has been extensively studied in mammals, leading to the conclusion that PTEN is a major tumor suppressor gene. PTEN [...] Read more.
The PTEN/PI3K/mTOR signal transduction pathway is involved in the regulation of biological processes such as metabolism, cell growth, cell proliferation, and apoptosis. This pathway has been extensively studied in mammals, leading to the conclusion that PTEN is a major tumor suppressor gene. PTEN orthologues have been characterized in a variety of organisms, both vertebrates and non-vertebrates, and studies of the associated PTEN/PI3K/mTOR pathway indicate that it is widely conserved. Studies in fungal systems indicated a role of PTEN in fungal defense mechanisms in Candida albicans, and in the developmental process of sporulation in Saccharomyces cerevisiae. The present study was aimed at investigating the role of the PTEN ortholog, ptn1, in Ustilago maydis, the pathogen of maize. U. maydis ptn1 mutant strains where ptn1 gene is deleted or overexpressed were examined for phenotypes associate with mating, virulence and spore formation. While the overexpression of ptn1 had no substantial effects on virulence, ptn1 deletion strains showed slight reductions in mating efficiency and significant reductions in virulence; tumor formation on stem and/or leaves were severely reduced. Moreover, tumors, when present, had significantly lower levels of mature teliospores, and the percent germination of such spores was similarly reduced. Thus, ptn1 is required for these important aspects of virulence in this fungus. Full article
(This article belongs to the Special Issue Regulation of Fungal Morphogenesis and Gene Expression)
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28 pages, 5307 KiB  
Article
PaPro1 and IDC4, Two Genes Controlling Stationary Phase, Sexual Development and Cell Degeneration in Podospora anserina
by Valérie Gautier, Laetitia Chan Ho Tong, Tinh-Suong Nguyen, Robert Debuchy and Philippe Silar
J. Fungi 2018, 4(3), 85; https://doi.org/10.3390/jof4030085 - 11 Jul 2018
Cited by 18 | Viewed by 4340
Abstract
Filamentous fungi frequently undergo bistable phenotypic switches. Crippled Growth of Podospora anserina is one such bistable switch, which seems to rely upon the mis-activation of a self-regulated PaMpk1 MAP kinase regulatory pathway. Here, we identify two new partners of this pathway: PaPro1, a [...] Read more.
Filamentous fungi frequently undergo bistable phenotypic switches. Crippled Growth of Podospora anserina is one such bistable switch, which seems to rely upon the mis-activation of a self-regulated PaMpk1 MAP kinase regulatory pathway. Here, we identify two new partners of this pathway: PaPro1, a transcription factor orthologous to Sordaria macrospora pro1 and Neurospora crassa ADV-1, and IDC4, a protein with an AIM24 domain. Both PaPro1 and IDC4 regulate stationary phase features, as described for the other actors of the PaMpk1 signaling pathway. However, PaPro1 is also involved in the control of fertilization by activating the transcription of the HMG8 and the mating type transcription factors, as well as the sexual pheromones and receptor genes. The roles of two components of the STRIPAK complex were also investigated by inactivating their encoding genes: PaPro22 and PaPro45. The mutants of these genes were found to have the same phenotypes as PaPro1 and IDC4 mutants as well as additional phenotypes including slow growth, abnormally shaped hyphae, pigment accumulation and blockage of the zygotic tissue development, indicating that the STRIPAK complex regulates, in addition to the PaMpk1 one, other pathways in P. anserina. Overall, the mutants of these four genes confirm the model by which Crippled Growth is due to the abnormal activation of the PaMpk1 MAP kinase cascade. Full article
(This article belongs to the Special Issue Regulation of Fungal Morphogenesis and Gene Expression)
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Review

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15 pages, 804 KiB  
Review
Regulation of Candida albicans Hyphal Morphogenesis by Endogenous Signals
by Daniel Kornitzer
J. Fungi 2019, 5(1), 21; https://doi.org/10.3390/jof5010021 - 28 Feb 2019
Cited by 58 | Viewed by 8009
Abstract
Candida albicans is a human commensal fungus that is able to assume several morphologies, including yeast, hyphal, and pseudohyphal. Under a range of conditions, C. albicans performs a regulated switch to the filamentous morphology, characterized by the emergence of a germ tube from [...] Read more.
Candida albicans is a human commensal fungus that is able to assume several morphologies, including yeast, hyphal, and pseudohyphal. Under a range of conditions, C. albicans performs a regulated switch to the filamentous morphology, characterized by the emergence of a germ tube from the yeast cell, followed by a mold-like growth of branching hyphae. This transition from yeast to hyphal growth has attracted particular attention, as it has been linked to the virulence of C. albicans as an opportunistic human pathogen. Signal transduction pathways that mediate the induction of the hyphal transcription program upon the imposition of external stimuli have been extensively investigated. However, the hyphal morphogenesis transcription program can also be induced by internal cellular signals, such as inhibition of cell cycle progression, and conversely, the inhibition of hyphal extension can repress hyphal-specific gene expression, suggesting that endogenous cellular signals are able to modulate hyphal gene expression as well. Here we review recent developments in the regulation of the hyphal morphogenesis of C. albicans, with emphasis on endogenous morphogenetic signals. Full article
(This article belongs to the Special Issue Regulation of Fungal Morphogenesis and Gene Expression)
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28 pages, 898 KiB  
Review
Linking Cellular Morphogenesis with Antifungal Treatment and Susceptibility in Candida Pathogens
by Jehoshua Sharma, Sierra Rosiana, Iqra Razzaq and Rebecca S. Shapiro
J. Fungi 2019, 5(1), 17; https://doi.org/10.3390/jof5010017 - 21 Feb 2019
Cited by 39 | Viewed by 8007
Abstract
Fungal infections are a growing public health concern, and an increasingly important cause of human mortality, with Candida species being amongst the most frequently encountered of these opportunistic fungal pathogens. Several Candida species are polymorphic, and able to transition between distinct morphological states, [...] Read more.
Fungal infections are a growing public health concern, and an increasingly important cause of human mortality, with Candida species being amongst the most frequently encountered of these opportunistic fungal pathogens. Several Candida species are polymorphic, and able to transition between distinct morphological states, including yeast, hyphal, and pseudohyphal forms. While not all Candida pathogens are polymorphic, the ability to undergo morphogenesis is linked with the virulence of many of these pathogens. There are also many connections between Candida morphogenesis and antifungal drug treatment and susceptibility. Here, we review how Candida morphogenesis—a key virulence trait—is linked with antifungal drugs and antifungal drug resistance. We highlight how antifungal therapeutics are able to modulate morphogenesis in both sensitive and drug-resistant Candida strains, the shared signaling pathways that mediate both morphogenesis and the cellular response to antifungal drugs and drug resistance, and the connection between Candida morphology, drug resistance, and biofilm growth. We further review the development of anti-virulence drugs, and targeting Candida morphogenesis as a novel therapeutic strategy to target fungal pathogens. Together, this review highlights important connections between fungal morphogenesis, virulence, and susceptibility to antifungals. Full article
(This article belongs to the Special Issue Regulation of Fungal Morphogenesis and Gene Expression)
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