scholarly journals Drosophila Model in the Study Role of UCH-L1

2018 ◽  
Author(s):  
Dang Thi Phuong Thao
Keyword(s):  
Drosophila Model

Speciation and changes in male gene expression in Drosophila

Genome ◽  
2020 ◽  
pp. 1-11
Author(s):  
Bahar Patlar ◽  
Alberto Civetta
Keyword(s):  
Gene Expression ◽  
Reproductive Isolation ◽  
Potential Role ◽  
Regulation Of Gene Expression ◽  
Drosophila Model ◽  
Depth Analysis ◽  
The Impact ◽  
Plastic Responses ◽  
Male Gene

It has long been acknowledged that changes in the regulation of gene expression may account for major organismal differences. However, we still do not fully understand how changes in gene expression evolve and how do such changes influence organisms’ differences. We are even less aware of the impact such changes might have in restricting gene flow between species. Here, we focus on studies of gene expression and speciation in the Drosophila model. We review studies that have identified gene interactions in post-mating reproductive isolation and speciation, particularly those that modulate male gene expression. We also address studies that have experimentally manipulated changes in gene expression to test their effect in post-mating reproductive isolation. We highlight the need for a more in-depth analysis of the role of selection causing disrupted gene expression of such candidate genes in sterile/inviable hybrids. Moreover, we discuss the relevance to incorporate more routinely assays that simultaneously evaluate the potential effects of environmental factors and genetic background in modulating plastic responses in male genes and their potential role in speciation.

scholarly journals The Drosophila Model: Exploring Novel Therapeutic Compounds against Neurodegenerative Diseases

Antioxidants ◽  
2019 ◽  
Vol 8 (12) ◽  
pp. 623 ◽  
Author(s):  
Sun Joo Cha ◽  
Hyeon-Ah Do ◽  
Hyun-Jun Choi ◽  
Mihye Lee ◽  
Kiyoung Kim
Keyword(s):  
Neurodegenerative Diseases ◽  
Fruits And Vegetables ◽  
Uv Light ◽  
Dietary Polyphenols ◽  
Drosophila Model ◽  
Therapeutic Compounds ◽  
Novel Drug ◽  
And Oxidative Stress ◽  
Drosophila Models

Polyphenols are secondary metabolites of plants, fruits, and vegetables. They act as antioxidants against free radicals from UV light, pathogens, parasites, and oxidative stress. In Drosophila models, feeding with various polyphenols results in increased antioxidant capacity and prolonged lifespan. Therefore, dietary polyphenols have several health advantages for preventing many human diseases, including cardiovascular diseases, cancer, and neurodegenerative diseases. However, the exact role of polyphenols in neurodegenerative diseases is still yet to be completely defined. This review focuses on the most recent studies related to the therapeutic effect of polyphenols in neurodegenerative disease management and provides an overview of novel drug discovery from various polyphenols using the Drosophila model.

scholarly journals ­Bcl-2 homologue debcl enhances α-synuclein-induced phenotypes in Drosophila

2016 ◽  
Author(s):  
Peter G M'Angale ◽  
Brian E Staveley
Keyword(s):  
Parkinson Disease ◽  
Dopaminergic Neurons ◽  
Neuronal Degeneration ◽  
Altered Expression ◽  
Drosophila Model ◽  
Age Dependent ◽  
Climbing Ability ◽  
The Common ◽  
Locomotor Ability

Background Parkinson disease (PD) is a debilitating movement disorder that afflicts 1 to 2% of the population over 50 years of age. The common hallmark for both sporadic and familial forms of PD is mitochondrial dysfunction. Mammals have at least twenty proapoptotic and antiapoptotic Bcl-2 family members, in contrast, only two Bcl-2 family genes have been identified in Drosophila melanogaster, the proapoptotic mitochondrial localized debcl and the antiapoptotic Buffy. The expression of α-synuclein, the first gene identified to contribute to inherited forms of PD, in the dopaminergic neurons (DA) of flies has provided a robust and well-studied Drosophila model of PD complete with the loss of neurons and accompanying motor defects. The altered expression of debcl in the DA neurons and neuron-rich eye and along with the expression of α-synuclein offers an opportunity to highlight the role of debcl in mitochondrial-dependent neuronal degeneration and death. Results The directed overexpression of debcl using the Ddc-Gal4 transgene in the dopaminergic neurons of Drosophila resulted in flies with severely decreased survival and a premature age-dependent loss in climbing ability. The inhibition of debcl resulted in enhanced survival and improved climbing ability whereas the overexpression of debcl in the α-synuclein-induced Drosophila model of PD resulted in more severe phenotypes. In addition, the co-expression of debcl along with Buffy partially counteracts the debcl-induced phenotypes, to improve the lifespan and the associated loss of locomotor ability observed. In complementary experiments, the overexpression of debcl along with the expression of α-synuclein in the eye, enhanced the eye ablation that results from the overexpression of debcl. The co-expression of Buffy along with debcl overexpression results in the rescue of the moderate developmental eye defects. The co-expression of Buffy along with inhibition of debcl partially restores the eye to a roughened eye phenotype. Discussion The overexpression of debcl in DA neurons produces flies with shortened lifespan and impaired locomotor ability, phenotypes that are strongly associated with models of PD in Drosophila. The co-expression of debcl along with α-synuclein enhanced the Parkinson disease-like phenotypes. The co-expression of debcl along with Buffy suppresses these phenotypes. Complementary experiments in the Drosophila eye show similar trends during development. Taken all together these results suggest a role for debcl in neurodegenerative disorders.

scholarly journals Haemocytes are critical for Drosophila melanogaster post-embryonic development, independent of control of the microbiota

2021 ◽  
Author(s):  
Holly N Stephenson ◽  
Robert Streeck ◽  
Alf Herzig
Keyword(s):  
Embryonic Development ◽  
Adult Development ◽  
Critical Role ◽  
Rna Seq ◽  
Genetic Rescue ◽  
Germ Free ◽  
Drosophila Model ◽  
Axenic Conditions ◽  
Driver Line

Proven roles for haemocytes (blood cells) have expanded beyond the control of infections in Drosophila. Despite this, the critical role of haemocytes in post-embryonic development has long been thought to be limited to control of microorganisms during metamorphosis. This has previously been shown by rescue of adult development in haemocyte-ablation models under germ-free conditions. Here we show that haemocytes have a critical role in post-embryonic development beyond their ability to control the microbiota. Using a newly generated, strong haemocyte-specific driver line for the GAL4/UAS system, we show that specific ablation of haemocytes is pupal lethal, even under axenic conditions. Genetic rescue experiments prove that this is a haemocyte-specific phenomena. RNA-seq data suggests that dysregulation of the midgut is a critical consequence of haemocyte ablation. We believe this novel role of haemocytes during metamorphosis is a major finding for the field. This is an exciting new Drosophila model to study the precise mechanisms in which haemocytes regulate tissue development, findings from which could have far reaching implications beyond invertebrate biology.

scholarly journals The Role of Gut Microbiota in Aging and Aging Related Neurodegenerative Disorders: Insights from Drosophila Model

Life ◽  
2021 ◽  
Vol 11 (8) ◽  
pp. 855
Author(s):  
Yan Kong ◽  
Liyuan Wang ◽  
Baichun Jiang
Keyword(s):  
Gut Microbiota ◽  
Neurodegenerative Disorders ◽  
Molecular Mechanisms ◽  
Physiological Function ◽  
Time Dependent ◽  
Model Organisms ◽  
Gi Tract ◽  
Drosophila Model ◽  
Increased Susceptibility

Aging is characterized by a time dependent impairment of physiological function and increased susceptibility to death. It is the major risk factor for neurodegeneration. Neurodegenerative disorders including Alzheimer’s disease (AD) and Parkinson’s disease (PD) are the main causes of dementia in the old population. Gut microbiota is a community of microorganisms colonized in the gastrointestinal (GI) tract. The alteration of gut microbiota has been proved to be associated with aging and aging related neurodegeneration. Drosophila is a powerful tool to study microbiota-mediated physiological and pathological functions. Here, we summarize the recent advances using Drosophila as model organisms to clarify the molecular mechanisms and develop a therapeutic method targeting microbiota in aging and aging-related neurodegenerative disorders.

scholarly journals Enhancer-Promoter Communication Is Regulated by Insulator Pairing in a Drosophila Model Bigenic Locus

2008 ◽  
Vol 28 (17) ◽  
pp. 5469-5477 ◽  
Author(s):  
Oksana Maksimenko ◽  
Anton Golovnin ◽  
Pavel Georgiev
Keyword(s):  
Functional Role ◽  
Negative Regulation ◽  
Loop Formation ◽  
Regulatory Systems ◽  
Drosophila Model ◽  
Study Support ◽  
Higher Eukaryotes ◽  
Insulator Elements ◽  
Target Promoters

ABSTRACT The complexity of regulatory systems in higher eukaryotes, featuring many distantly located enhancers that nonetheless properly activate the target promoters, has prompted the hypothesis that the action of enhancers should be restricted by insulators. Continuing our research on the functional role of insulators and the consequences of their interaction in Drosophila, we studied the interplay of different Su(Hw)-dependent Drosophila insulators. The set of transgenic constructs comprised two consecutive genes (yellow and white) with their enhancers and insulator elements differently arranged in between and/or around the gene(s). All insulators were found to interact in twin or mixed tandems, demonstrating the bypass phenomenon. However, insulator pairing around a gene did not always improve its isolation from an outside enhancer. On the other hand, merely two insulator elements (identical or different) in appropriate positions can permit the expression of one gene but not the gene next to it or, conversely, largely block the transcription of the first gene, while allowing full enhancement of the second, or make them behave similarly. Thus, the results of this study support the model that loop formation by insulators is an essential component of insulator action on a positive and negative regulation of an enhancer-promoter communication.

Presynaptic dysfunction in Huntington's disease

2010 ◽  
Vol 38 (2) ◽  
pp. 488-492 ◽  
Author(s):  
José L. Rozas ◽  
Leonardo Gómez-Sánchez ◽  
Cristina Tomás-Zapico ◽  
José J. Lucas ◽  
Rafael Fernández-Chacón
Keyword(s):  
Huntington's Disease ◽  
Huntington’S Disease ◽  
Molecular Mechanisms ◽  
Neuronal Damage ◽  
Motor Dysfunction ◽  
Drosophila Model ◽  
Glutamine Repeat ◽  
Mutant Forms ◽  
The Relationship

HD (Huntington's disease) is produced by the expression of mutant forms of the protein htt (huntingtin) containing a pathologically expanded poly-glutamine repeat. For unknown reasons, in HD patients and HD mouse models, neurons from the striatum and cerebral cortex degenerate and lead to motor dysfunction and dementia. Synaptic transmission in those neurons becomes progressively altered during the course of the disease. However, the relationship between synaptic dysfunction and neurodegeneration in HD is not yet clear. Are there early specific functional synaptic changes preceding symptoms and neurodegeneration? What is the role of those changes in neuronal damage? Recent experiments in a Drosophila model of HD have showed that abnormally increased neurotransmitter release might be a leading cause of neurodegeneration. In the present review, we summarize recently described synaptic alterations in HD animal models and discuss potential underlying molecular mechanisms.

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