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Drosophila Models of Development and Disease
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Drosophila Models of Development and Disease

A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Cellular Pathology".

Deadline for manuscript submissions: closed (20 December 2023) | Viewed by 3533

Special Issue Editor

Dr. Aiguo Tian

E-Mail Website
Guest Editor
Department of Biochemistry and Molecular Biology, Tulane University School of Medicine, Louisiana Cancer Research Center, New Orleans, LA 70112, USA
Interests: intestine stem cells; tissue damage; homeostasis and regeneration; epithelial tumors and cell polarity
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Since Thomas Hunt Morgan and his students performed pioneering work using fruit flies to demonstrate that genes are located on chromosomes, as well as provided the first evidence for the concept of gene linkage, the fruit fly has been extensively used as a model organism for over a century to study a wide range of biological processes, including genetics, embryonic development, stem cells and organ regeneration, behavior, aging, among others. In addition, approximately 75% of all human disease-related genes have functional homologs in the fruit fly. Coupled with its low genetic redundancy, the fruit fly has been used to address specific questions about human diseases, such as neurological disorders, cancer, cardiovascular disease, metabolic and storage diseases, and more. By studying the molecular and cellular mechanisms of these diseases in the fruit fly, researchers can gain new insights into the underlying causes of disease and develop new strategies for treatment.

This Special Issue of the Journal of Cells will feature review-type articles and original research that highlight the power of Drosophila research in many aspects of development and human disease modeling.

Dr. Aiguo Tian
Guest Editor

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. Cells is an international peer-reviewed open access semimonthly 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 2700 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

  • drosophila
  • developmental biology
  • diseases

Published Papers (3 papers)

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Research

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21 pages, 4423 KiB  
Article
Anti-Tumor Effect of Turandot Proteins Induced via the JAK/STAT Pathway in the mxc Hematopoietic Tumor Mutant in Drosophila
by Yuriko Kinoshita, Naoka Shiratsuchi, Mayo Araki and Yoshihiro H. Inoue
Cells 2023, 12(16), 2047; https://doi.org/10.3390/cells12162047 - 11 Aug 2023
Cited by 1 | Viewed by 1271
Abstract
Several antimicrobial peptides suppress the growth of lymph gland (LG) tumors in Drosophila multi sex comb (mxc) mutant larvae. The activity of another family of polypeptides, called Turandots, is also induced via the JAK/STAT pathway after bacterial infection; however, their influence [...] Read more.
Several antimicrobial peptides suppress the growth of lymph gland (LG) tumors in Drosophila multi sex comb (mxc) mutant larvae. The activity of another family of polypeptides, called Turandots, is also induced via the JAK/STAT pathway after bacterial infection; however, their influence on Drosophila tumors remains unclear. The JAK/STAT pathway was activated in LG tumors, fat body, and circulating hemocytes of mutant larvae. The mRNA levels of Turandot (Tot) genes increased markedly in the mutant fat body and declined upon silencing Stat92E in the fat body, indicating the involvement of the JAK/STAT pathway. Furthermore, significantly enhanced tumor growth upon a fat-body-specific silencing of the mRNAs demonstrated the antitumor effects of these proteins. The proteins were found to be incorporated into small vesicles in mutant circulating hemocytes (as previously reported for several antimicrobial peptides) but not normal cells. In addition, more hemocytes containing these proteins were found to be associated with tumors. The mutant LGs contained activated effector caspases, and a fat-body-specific silencing of Tots inhibited apoptosis and increased the number of mitotic cells in the LG, thereby suggesting that the proteins inhibited tumor cell proliferation. Thus, Tot proteins possibly exhibit antitumor effects via the induction of apoptosis and inhibition of cell proliferation. Full article
(This article belongs to the Special Issue Drosophila Models of Development and Disease)
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12 pages, 1323 KiB  
Article
The Comet Assay in Drosophila: A Tool to Study Interactions between DNA Repair Systems in DNA Damage Responses In Vivo and Ex Vivo
by Rubén Rodríguez, Isabel Gaivão, Leticia Aguado, Marta Espina, Jorge García, Pablo Martínez-Camblor and L. María Sierra
Cells 2023, 12(15), 1979; https://doi.org/10.3390/cells12151979 - 31 Jul 2023
Cited by 1 | Viewed by 1155
Abstract
The comet assay in Drosophila has been used in the last few years to study DNA damage responses (DDR) in different repair-mutant strains and to compare them to analyze DNA repair. We have used this approach to study interactions between DNA repair pathways [...] Read more.
The comet assay in Drosophila has been used in the last few years to study DNA damage responses (DDR) in different repair-mutant strains and to compare them to analyze DNA repair. We have used this approach to study interactions between DNA repair pathways in vivo. Additionally, we have implemented an ex vivo comet assay, in which nucleoids from treated and untreated cells were incubated ex vivo with cell-free protein extracts from individuals with distinct repair capacities. Four strains were used: wild-type OregonK (OK), nucleotide excision repair mutant mus201, dmPolQ protein mutant mus308, and the double mutant mus201;mus308. Methyl methanesulfonate (MMS) was used as a genotoxic agent. Both approaches were performed with neuroblasts from third-instar larvae; they detected the effects of the NER and dmPolQ pathways on the DDR to MMS and that they act additively in this response. Additionally, the ex vivo approach quantified that mus201, mus308, and the double mutant mus201;mus308 strains presented, respectively, 21.5%, 52.9%, and 14.8% of OK strain activity over MMS-induced damage. Considering the homology between mammals and Drosophila in repair pathways, the detected additive effect might be extrapolated even to humans, demonstrating that Drosophila might be an excellent model to study interactions between repair pathways. Full article
(This article belongs to the Special Issue Drosophila Models of Development and Disease)
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Review

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21 pages, 2210 KiB  
Review
Drosophila Contributions towards Understanding Neurofibromatosis 1
by Kalliopi Atsoniou, Eleni Giannopoulou, Eirini-Maria Georganta and Efthimios M. C. Skoulakis
Cells 2024, 13(8), 721; https://doi.org/10.3390/cells13080721 - 21 Apr 2024
Viewed by 676
Abstract
Neurofibromatosis 1 (NF1) is a multisymptomatic disorder with highly variable presentations, which include short stature, susceptibility to formation of the characteristic benign tumors known as neurofibromas, intense freckling and skin discoloration, and cognitive deficits, which characterize most children with the condition. Attention deficits [...] Read more.
Neurofibromatosis 1 (NF1) is a multisymptomatic disorder with highly variable presentations, which include short stature, susceptibility to formation of the characteristic benign tumors known as neurofibromas, intense freckling and skin discoloration, and cognitive deficits, which characterize most children with the condition. Attention deficits and Autism Spectrum manifestations augment the compromised learning presented by most patients, leading to behavioral problems and school failure, while fragmented sleep contributes to chronic fatigue and poor quality of life. Neurofibromin (Nf1) is present ubiquitously during human development and postnatally in most neuronal, oligodendrocyte, and Schwann cells. Evidence largely from animal models including Drosophila suggests that the symptomatic variability may reflect distinct cell-type-specific functions of the protein, which emerge upon its loss, or mutations affecting the different functional domains of the protein. This review summarizes the contributions of Drosophila in modeling multiple NF1 manifestations, addressing hypotheses regarding the cell-type-specific functions of the protein and exploring the molecular pathways affected upon loss of the highly conserved fly homolog dNf1. Collectively, work in this model not only has efficiently and expediently modelled multiple aspects of the condition and increased understanding of its behavioral manifestations, but also has led to pharmaceutical strategies towards their amelioration. Full article
(This article belongs to the Special Issue Drosophila Models of Development and Disease)
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