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Drosophila: A Genetic Model for Studying Human Diseases
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Drosophila: A Genetic Model for Studying Human Diseases

A special issue of Genes (ISSN 2073-4425). This special issue belongs to the section "Human Genomics and Genetic Diseases".

Deadline for manuscript submissions: closed (20 July 2023) | Viewed by 7203

Special Issue Editors

Dr. Sergio Casas-Tintó

E-Mail Website
Guest Editor
IIER- ISCIII, Majadahonda 28220 Madrid, Spain
Interests: Drosophila; neurodegeneration; cancer; genetics; behaviour; disease; development
Special Issues, Collections and Topics in MDPI journals
Dr. Luis Alberto Baena-López

E-Mail Website
Guest Editor
Sir William Dunn School of Pathology, University of Oxford, South Parks Road, Oxford OX1 3RE, UK
Interests: Drosophila; caspase biology; cancer; genetics; genome editing; disease; stem cell regulation

Special Issue Information

Dear Colleagues,

In recent decades, we have achieved great advances in the investigation of the cellular and molecular processes that underlie human disease. Studies conducted in different model organisms including Drosophila melanogaster are rapidly improving our basic understanding regarding the cellular and molecular principles of human disease. Specifically, the powerful genetic toolbox, tissue accessibility, short lifecycle, and large progeny have conferred to fruit flies a central role in the investigation of the origins of human disease. These features of Drosophila have been instrumental to generate preclinical settings to uncover novel therapeutic approaches. Therefore, Drosophila plays a central role in the study of the mechanisms involved in disease progression, and the efficient screening for candidate targets and preclinical studies. It is well known that Drosophila as an experimental model has unique genetic tools that allow the fine-tuning of gene expression and therefore can mimic different complex pathological conditions. In addition, the high conservation of genes involved in human disease makes Drosophila an advantageous animal model to study human disease. These features have been instrumental to generating preclinical settings to uncover novel therapeutic approaches.

This Special Issue aims to illustrate how this insect has helped us to model and even alleviate numerous human pathologies such as cancer, neurological diseases, or metabolic disorders.

Dr. Sergio Casas-Tintó
Dr. Luis Alberto Baena-López
Guest Editors

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Genes is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2600 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • Disease
  • Animal model
  • Neurodegeneration
  • Neuromuscular
  • Metabolic
  • Cancer
  • Learning and memory

Published Papers (3 papers)

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Research

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18 pages, 8286 KiB  
Article
Drosophila as Model System to Study Ras-Mediated Oncogenesis: The Case of the Tensin Family of Proteins
by Ana Martínez-Abarca Millán, Jennifer Soler Beatty, Andrea Valencia Expósito and María D. Martín-Bermudo
Genes 2023, 14(7), 1502; https://doi.org/10.3390/genes14071502 - 23 Jul 2023
Viewed by 1346
Abstract
Oncogenic mutations in the small GTPase Ras contribute to ~30% of human cancers. However, tissue growth induced by oncogenic Ras is restrained by the induction of cellular senescence, and additional mutations are required to induce tumor progression. Therefore, identifying cooperating cancer genes is [...] Read more.
Oncogenic mutations in the small GTPase Ras contribute to ~30% of human cancers. However, tissue growth induced by oncogenic Ras is restrained by the induction of cellular senescence, and additional mutations are required to induce tumor progression. Therefore, identifying cooperating cancer genes is of paramount importance. Recently, the tensin family of focal adhesion proteins, TNS1-4, have emerged as regulators of carcinogenesis, yet their role in cancer appears somewhat controversial. Around 90% of human cancers are of epithelial origin. We have used the Drosophila wing imaginal disc epithelium as a model system to gain insight into the roles of two orthologs of human TNS2 and 4, blistery (by) and PVRAP, in epithelial cancer progression. We have generated null mutations in PVRAP and found that, as is the case for by and mammalian tensins, PVRAP mutants are viable. We have also found that elimination of either PVRAP or by potentiates RasV12-mediated wing disc hyperplasia. Furthermore, our results have unraveled a mechanism by which tensins may limit Ras oncogenic capacity, the regulation of cell shape and growth. These results demonstrate that Drosophila tensins behave as suppressors of Ras-driven tissue hyperplasia, suggesting that the roles of tensins as modulators of cancer progression might be evolutionarily conserved. Full article
(This article belongs to the Special Issue Drosophila: A Genetic Model for Studying Human Diseases)
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Review

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21 pages, 9103 KiB  
Review
Relating the Biogenesis and Function of P Bodies in Drosophila to Human Disease
by Elise L. Wilby and Timothy T. Weil
Genes 2023, 14(9), 1675; https://doi.org/10.3390/genes14091675 - 24 Aug 2023
Viewed by 1418
Abstract
Drosophila has been a premier model organism for over a century and many discoveries in flies have furthered our understanding of human disease. Flies have been successfully applied to many aspects of health-based research spanning from behavioural addiction, to dysplasia, to RNA dysregulation [...] Read more.
Drosophila has been a premier model organism for over a century and many discoveries in flies have furthered our understanding of human disease. Flies have been successfully applied to many aspects of health-based research spanning from behavioural addiction, to dysplasia, to RNA dysregulation and protein misfolding. Recently, Drosophila tissues have been used to study biomolecular condensates and their role in multicellular systems. Identified in a wide range of plant and animal species, biomolecular condensates are dynamic, non-membrane-bound sub-compartments that have been observed and characterised in the cytoplasm and nuclei of many cell types. Condensate biology has exciting research prospects because of their diverse roles within cells, links to disease, and potential for therapeutics. In this review, we will discuss processing bodies (P bodies), a conserved biomolecular condensate, with a particular interest in how Drosophila can be applied to advance our understanding of condensate biogenesis and their role in disease. Full article
(This article belongs to the Special Issue Drosophila: A Genetic Model for Studying Human Diseases)
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14 pages, 2660 KiB  
Review
Drosophila melanogaster as a Model to Study Fragile X-Associated Disorders
by Jelena Trajković, Vedrana Makevic, Milica Pesic, Sofija Pavković-Lučić, Sara Milojevic, Smiljana Cvjetkovic, Randi Hagerman, Dejan B. Budimirovic and Dragana Protic
Genes 2023, 14(1), 87; https://doi.org/10.3390/genes14010087 - 28 Dec 2022
Viewed by 3654
Abstract
Fragile X syndrome (FXS) is a global neurodevelopmental disorder caused by the expansion of CGG trinucleotide repeats (≥200) in the Fragile X Messenger Ribonucleoprotein 1 (FMR1) gene. FXS is the hallmark of Fragile X-associated disorders (FXD) and the most common monogenic [...] Read more.
Fragile X syndrome (FXS) is a global neurodevelopmental disorder caused by the expansion of CGG trinucleotide repeats (≥200) in the Fragile X Messenger Ribonucleoprotein 1 (FMR1) gene. FXS is the hallmark of Fragile X-associated disorders (FXD) and the most common monogenic cause of inherited intellectual disability and autism spectrum disorder. There are several animal models used to study FXS. In the FXS model of Drosophila, the only ortholog of FMR1, dfmr1, is mutated so that its protein is missing. This model has several relevant phenotypes, including defects in the circadian output pathway, sleep problems, memory deficits in the conditioned courtship and olfactory conditioning paradigms, deficits in social interaction, and deficits in neuronal development. In addition to FXS, a model of another FXD, Fragile X-associated tremor/ataxia syndrome (FXTAS), has also been established in Drosophila. This review summarizes many years of research on FXD in Drosophila models. Full article
(This article belongs to the Special Issue Drosophila: A Genetic Model for Studying Human Diseases)
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