Endoplasmic reticulum stress and fungal pathogenesis |
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| Institution: | 1. Department of Biological Chemistry, University of California, Irvine, Irvine, CA 92697, USA;2. Division of Infectious Diseases, Los Angeles Biomedical Research Institute at Harbor-UCLA Medical Center, Torrance, CA 90502, USA;3. David Geffen School of Medicine at UCLA, Los Angeles, CA 90024, USA;1. Laboratory of Molecular Microbiology, Graduate School of Bioagricultural Sciences, Nagoya University, Chikusa-ku, Nagoya 464-8601, Japan;2. Laboratory of Molecular Microbiology, Department of Basic Medicinal Sciences, Graduate School of Pharmaceutical Sciences, Nagoya University, Chikusa-ku, Nagoya 464-8601, Japan;3. Department of Biological Science, Faculty of Science and Engineering, Chuo University, 1-13-27 Kasuga, Bunkyo-ku, Tokyo 112-8551, Japan;1. Faculdade de Ciências Farmacêuticas de Ribeirão Preto, Universidade de São Paulo, São Paulo, Brazil;2. Laboratório Nacional de Ciência e Tecnologia do Bioetanol (CTBE), Campinas, Brazil;1. Department of Pediatrics, Division of Pediatric Infectious Diseases, Duke University Medical Center, Durham, NC, USA;2. Infectious Diseases Service, Department of Medicine, Lausanne University Hospital, Lausanne, Switzerland;3. Institute of Microbiology, Lausanne University Hospital, Lausanne, Switzerland;4. Department of Molecular Genetics and Microbiology, Duke University Medical Center, Durham, NC, USA |
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| Abstract: | The gateway to the secretory pathway is the endoplasmic reticulum (ER), an organelle that is responsible for the accurate folding, post-translational modification and final assembly of up to a third of the cellular proteome. When secretion levels are high, errors in protein biogenesis can lead to the accumulation of abnormally folded proteins, which threaten ER homeostasis. The unfolded protein response (UPR) is an adaptive signaling pathway that counters a buildup in misfolded and unfolded proteins by increasing the expression of genes that support ER protein folding capacity. Fungi, like other eukaryotic cells that are specialized for secretion, rely upon the UPR to buffer ER stress caused by fluctuations in secretory demand. However, emerging evidence is also implicating the UPR as a central regulator of fungal pathogenesis. In this review, we discuss how diverse fungal pathogens have adapted ER stress response pathways to support the expression of virulence-related traits that are necessary in the host environment. |
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| Keywords: | ER stress Fungal pathogenesis Fungal virulence Hac1 HacA Ire1 IreA Unfolded protein response UPR |
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