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Simple Organisms for Complex Problems: Modeling Human Disease in Yeast...
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Simple Organisms for Complex Problems: Modeling Human Disease in Yeast and Dictyostelium II

A special issue of Cells (ISSN 2073-4409).

Deadline for manuscript submissions: closed (30 November 2023) | Viewed by 3301

Special Issue Editor

Dr. Ricardo Escalante

E-Mail Website
Guest Editor
Biomedical Research Institute (IIB), Arturo Duperier 4, 28029 Madrid, Spain
Interests: autophagy; Dictyostelium; membrane trafficking
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

The molecular pathways and mechanisms involved in human diseases are often conserved in simple eukaryotes. Microbial models, such as the yeast Saccharomyces cerevisiae and the social amoeba Dictyostelium discoideum, have traditionally been used in basic science to contribute to a better understanding of living organisms. Today, however, the boundaries of basic and applied science are blurring. Understanding the molecular mechanisms involved in diseases requires ever-deeper knowledge at the molecular level. In addition, the discovery of the underlying genetic cause of many rare diseases requires further investigation of the basic function of many as-yet poorly characterized genes, proteins and signaling pathways. Infectious diseases also benefit from the use of simple models to uncover the interaction between hosts and pathogens. In this complex scenario, the use of simple organisms as disease models is increasingly necessary to unravel intricate pathological mechanisms that could aid in the design of new knowledge-based therapies.

In this Special Issue we welcome contributions focused on the use of eukaryote microorganisms, such as Saccharomyces cerevisiae and Dictyostelium discoideum, to understand the molecular basis of human diseases.

Dr. Ricardo Escalante
Guest Editor

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Keywords

  • Dictyostelium discoideum
  • Saccharomyces cerevisiae
  • human disease
  • model organisms

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Published Papers (3 papers)

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Research

32 pages, 10052 KiB  
Article
The Multifaceted Interactions of Dictyostelium Atg1 with Mitochondrial Function, Endocytosis, Growth, and Development
by Melodi Gizem Sen, Oana Sanislav, Paul Robert Fisher and Sarah Jane Annesley
Cells 2024, 13(14), 1191; https://doi.org/10.3390/cells13141191 - 14 Jul 2024
Viewed by 459
Abstract
Autophagy is a degradative recycling process central to the maintenance of homeostasis in all eukaryotes. By ensuring the degradation of damaged mitochondria, it plays a key role in maintaining mitochondrial health and function. Of the highly conserved autophagy proteins, autophagy-related protein 1 (Atg1) [...] Read more.
Autophagy is a degradative recycling process central to the maintenance of homeostasis in all eukaryotes. By ensuring the degradation of damaged mitochondria, it plays a key role in maintaining mitochondrial health and function. Of the highly conserved autophagy proteins, autophagy-related protein 1 (Atg1) is essential to the process. The involvement of these proteins in intracellular signalling pathways, including those involving mitochondrial function, are still being elucidated. Here the role of Atg1 was investigated in the simple model organism Dictyostelium discoideum using an atg1 null mutant and mutants overexpressing or antisense-inhibiting atg1. When evaluated against the well-characterised outcomes of mitochondrial dysfunction in this model, altered atg1 expression resulted in an unconventional set of phenotypic outcomes in growth, endocytosis, multicellular development, and mitochondrial homeostasis. The findings here show that Atg1 is involved in a tightly regulated signal transduction pathway coordinating energy-consuming processes such as cell growth and multicellular development, along with nutrient status and energy production. Furthermore, Atg1’s effects on energy homeostasis indicate a peripheral ancillary role in the mitochondrial signalling network, with effects on energy balance rather than direct effects on electron transport chain function. Further research is required to tease out these complex networks. Nevertheless, this study adds further evidence to the theory that autophagy and mitochondrial signalling are not opposing but rather linked, yet strictly controlled, homeostatic mechanisms. Full article
(This article belongs to the Special Issue Simple Organisms for Complex Problems: Modeling Human Disease in Yeast and Dictyostelium II)
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23 pages, 12021 KiB  
Article
Polycystin-2 Mediated Calcium Signalling in the Dictyostelium Model for Autosomal Dominant Polycystic Kidney Disease
by Claire Y. Allan, Oana Sanislav and Paul R. Fisher
Cells 2024, 13(7), 610; https://doi.org/10.3390/cells13070610 - 31 Mar 2024
Viewed by 1144
Abstract
Autosomal dominant polycystic kidney disease (ADPKD) occurs when the proteins Polycystin-1 (PC1, PKD1) and Polycystin-2 (PC2, PKD2) contain mutations. PC1 is a large membrane receptor that can interact and form a complex with the calcium-permeable cation channel PC2. This complex localizes [...] Read more.
Autosomal dominant polycystic kidney disease (ADPKD) occurs when the proteins Polycystin-1 (PC1, PKD1) and Polycystin-2 (PC2, PKD2) contain mutations. PC1 is a large membrane receptor that can interact and form a complex with the calcium-permeable cation channel PC2. This complex localizes to the plasma membrane, primary cilia and ER. Dysregulated calcium signalling and consequential alterations in downstream signalling pathways in ADPKD are linked to cyst formation and expansion; however, it is not completely understood how PC1 and PC2 regulate calcium signalling. We have studied Polycystin-2 mediated calcium signalling in the model organism Dictyostelium discoideum by overexpressing and knocking down the expression of the endogenous Polycystin-2 homologue, Polycystin-2. Chemoattractant-stimulated cytosolic calcium response magnitudes increased and decreased in overexpression and knockdown strains, respectively, and analysis of the response kinetics indicates that Polycystin-2 is a significant contributor to the control of Ca2+ responses. Furthermore, basal cytosolic calcium levels were reduced in Polycystin-2 knockdown transformants. These alterations in Ca2+ signalling also impacted other downstream Ca2+-sensitive processes including growth rates, endocytosis, stalk cell differentiation and spore viability, indicating that Dictyostelium is a useful model to study Polycystin-2 mediated calcium signalling. Full article
(This article belongs to the Special Issue Simple Organisms for Complex Problems: Modeling Human Disease in Yeast and Dictyostelium II)
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16 pages, 3103 KiB  
Article
Suggesting Dictyostelium as a Model for Disease-Related Protein Studies through Myosin II Polymerization Pathway
by Xiong Liu and Shi Shu
Cells 2024, 13(3), 263; https://doi.org/10.3390/cells13030263 - 31 Jan 2024
Viewed by 927
Abstract
Dictyostelium myosin II displays remarkable dynamism within the cell, continually undergoing polymerization and depolymerization processes. Under low-ion conditions, it assumes a folded structure like muscle myosins and forms thick filaments through polymerization. In our study, we presented intermediate structures observed during the early [...] Read more.
Dictyostelium myosin II displays remarkable dynamism within the cell, continually undergoing polymerization and depolymerization processes. Under low-ion conditions, it assumes a folded structure like muscle myosins and forms thick filaments through polymerization. In our study, we presented intermediate structures observed during the early stages of polymerization of purified myosin via negative staining electron microscopy, immediately crosslinked with glutaraldehyde at the onset of polymerization. We identified folded monomers, dimers, and tetramers in the process. Our findings suggest that Dictyostelium myosin II follows a polymerization pathway in vitro akin to muscle myosin, with folded monomers forming folded parallel and antiparallel dimers that subsequently associate to create folded tetramers. These folded tetramers eventually unfold and associate with other tetramers to produce long filaments. Furthermore, our research revealed that ATP influences filament size, reducing it regardless of the status of RLC phosphorylation while significantly increasing the critical polymerization concentrations from 0.2 to 9 nM. In addition, we demonstrate the morphology of fully matured Dictyostelium myosin II filaments. Full article
(This article belongs to the Special Issue Simple Organisms for Complex Problems: Modeling Human Disease in Yeast and Dictyostelium II)
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