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This workshop will provide an introduction to peer reviewing for early career researchers, including graduate students.

Strategies for resistance to fungal pathogens

The workshop will cover best practices and a mock review. Becoming a better reviewer will help you to become a better author and to hone some of the skills central to scientific success, including critical thinking, evaluating research, providing helpful feedback, and understanding the mindset and expectations of peer reviewers and editors. A general discussion will follow the introductions based on the questions below. Do they initiate the process of invasive growth? And, more broadly, how is spatial organization of the hyphal cortex actually controlled?

Is it a consequence of gradients of endocytotic and exocytotic activity that provide longitudinal co-ordinates along a hypha thereby facilitating septin aggregation at correct locations, or is this instead an intrinsic characteristic of septins themselves, as suggested by in vitro studies Bridges and Gladfelter, It is clear that to answer such questions, the roles of septins in focused invasion and generation of cellular protrusions will need to be explored in much greater detail.

To achieve this, there is, for example, a need for specific analysis of septin function by generation of conditional mutants, or by conditional inhibition of septin aggregation during the infection process. The use of gene silencing or conditional alleles of septin genes may offer the means to do this most effectively, so that septin assembly can be prevented directly at the point of primary host infection, or later during invasive growth. The dynamics of septin assembly within living fungal cells during the infection process also requires further analysis.

This is, of course, challenging because it depends on the ability to conditionally manipulate septins, while at the same time carrying out live cell imaging. However, this is not beyond the scope of current methodologies, such as super-resolution microscopy, while correlative light and electron microscopy could provide ultrastructural analysis of such assemblies, followed by cryo-electron microscopy to study in vivo assembly dynamics in unparalleled detail.

Topic Area Bibliographies

Deployment of these approaches in pathogenic fungi undergoing host infection, will allow a comprehensive testing of our hypothesis that septins prevent aberrant polar outgrowths and thereby focus fungal invasive force at appropriate points for substrate invasion and fungal pathogenesis. An exciting prospect. MM and NT synthesized source material, generated ideas and conclusions, and co-authored the mini-review. The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

Alvarez-Tabares, I. Septins from the phytopathogenic fungus Ustilago maydis are required for proper morphogenesis but dispensable for virulence.

Berepiki, A. Septins are important for cell polarity, septation and asexual spore formation in Neurospora crassa and show different patterns of localisation at germ tube tips. Bridges, A. Fungal pathogens are platforms for discovering novel and conserved septin properties. In vitro reconstitution of septin assemblies on supported lipid bilayers. Methods Cell Biol.

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Micron-scale plasma membrane curvature is recognized by the septin cytoskeleton. Cell Biol. Brown, G. Hidden killers: human fungal infections. Chen, A. Septins are involved in nuclear division, morphogenesis and pathogenicity in Fusarium graminearum. Fungal Genet. Dagdas, Y. Septin-mediated plant cell invasion by the rice blast fungus, Magnaporthe oryzae.

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Science , — Douglas, L. Septin function in yeast model systems and pathogenic fungi. Eukaryotic Cell 4, — Emmett, R. Fisher, M. Tackling emerging fungal threats to animal health, food security and ecosystem resilience. B Gladfelter, A. Control of filamentous fungal cell shape by septins and formins.


Guides to the final frontier of the cytoskeleton: septins in filamentous fungi. Hajek, A. Leger, R. Interactions between fungal pathogens and insect hosts. Helfer, H. AgSwe1p regulates mitosis in response to morphogenesis and nutrients in multinucleated A. Cell 17, — Hernandez-Rodriguez, Y. Posttranslational modifications and assembly of septin heteropolymers and higher-order structures.

The septin AspB in Aspergillus nidulans forms bars and filaments and plays roles in growth emergence and conidiation. Eukaryotic Cell 11, — Distinct septin heteropolymers co-exist during multicellular development in the filamentous fungus Aspergillus nidulans. Joo, E. Septins: traffic control at the cytokinesis intersection.

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Traffic 6, — Khan, A. Septins and generation of asymmetries in fungal cells. Kozubowski, L. Septins enforce morphogenetic events during sexual reproduction and contribute to virulence of Cryptococcus neoformans. Lichius, A. Form follows function — the versatile fungal cytoskeleton. Fungal Biol. Lindsey, R.

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Septin localization across kingdoms: three themes with variations. Septins AspA and AspC are important for normal development and limit the emergence of new growth foci in the multicellular fungus Aspergillus nidulans. Eukaryotic Cell 9, — Mendgen, K. Infection structures of fungal plant pathogens — a cytological and physiological evaluation. New Phytol. Studies conducted primarily in the 2 model organisms Saccharomyces cerevisiae and Aspergillus nidulans have cemented our understanding of how fungi sense and respond to pH. More recently, pH has emerged as a key player in the control of fungal pathogenicity.

Infections caused by fungi are often associated with a pH shift in the surrounding host tissue [ 2 — 4 ]. Extracellular alkalinization contributes to fungal virulence, but the underlying mechanisms are not fully understood. Recent studies have revealed new and unexpected ways by which fungi induce host alkalinization to increase their infectious potential. Here, we provide a brief overview of the mechanisms that govern pH signaling in fungi and highlight how recent findings have advanced our understanding of pathogen-induced alkalinization and its role during infection.

We also discuss the emerging view that intracellular pH pHi acts as a master switch to govern fungal development and pathogenicity. High pH imposes severe stress on the fungal cell, including difficulties in the acquisition of nutrients or reduced availability of essential elements, such as iron or copper [ 5 ]. Recent work in S. Processed PacC protein functions both as an activator of alkaline-expressed genes and a repressor of acidic-expressed genes, thereby orchestrating the cellular response to alkaline pH [ 6 ].

Ambient pH adaptation ensures the expression of the adequate set of genes at a given pH. This is crucial during fungal infection to ensure, for example, the correct deployment of virulence factors that function at a specific pH [ 2 , 8 , 9 ]. In plant pathogenic fungi, PacC contributes to virulence in necrotrophic or postharvest pathogens [ 12 — 14 ] but is dispensable in others, such as the hemibiotrophic root-infecting fungus F.

List of model organisms

These results reveal contrasting roles of PacC, most likely associated with distinct modes of host infection of the different phytopathogens. Fungal pathogens have been known for decades to adjust the extracellular pH in order to increase their infectious potential [ 3 , 16 ]. Alkalinization of the plant host was first reported in a number of fruit-infecting species, such as Colletotrichum spp.

These fungi are able to trigger an increase of more than 2 units in the pH of the surrounding fruit tissue or the rhizosphere, respectively. Similarly, the human pathogen C.