Genome-wide analysis of phenobarbital-inducible genes in Drosophila melanogaster

2006 ◽  
Vol 15 (4) ◽  
pp. 455-464 ◽  
Author(s):  
W. Sun ◽  
V. M. Margam ◽  
L. Sun ◽  
G. Buczkowski ◽  
G. W. Bennett ◽  
...  
2006 ◽  
Vol 38 (6) ◽  
pp. 700-705 ◽  
Author(s):  
Yuri B Schwartz ◽  
Tatyana G Kahn ◽  
David A Nix ◽  
Xiao-Yong Li ◽  
Richard Bourgon ◽  
...  

2010 ◽  
Vol 21 (2) ◽  
pp. 182-192 ◽  
Author(s):  
R. A. Hoskins ◽  
J. M. Landolin ◽  
J. B. Brown ◽  
J. E. Sandler ◽  
H. Takahashi ◽  
...  

2015 ◽  
Vol 6 (1) ◽  
Author(s):  
Adam J. Dobson ◽  
John M. Chaston ◽  
Peter D. Newell ◽  
Leanne Donahue ◽  
Sara L. Hermann ◽  
...  

2001 ◽  
Vol 109 (2) ◽  
pp. 371-375 ◽  
Author(s):  
Frédéric Crémazy ◽  
Philippe Berta ◽  
Franck Girard

Genetics ◽  
2021 ◽  
Author(s):  
Jacinta Davis ◽  
Claire Da Silva Santos ◽  
Narda Caudillo Zavala ◽  
Nicholas Gans ◽  
Daniel Patracuolla ◽  
...  

Abstract Parkinson’s Disease (PD) is primarily characterized by the loss of dopaminergic (DA) neurons in the brain. However, little is known about why DA neurons are selectively vulnerable to PD. To identify genes that are associated with DA neuron loss, we screened through 201 wild-caught populations of Drosophila melanogaster as part of the Drosophila Genetic Reference Panel (DGRP). Here we identify the top associated genes containing SNPs that render DA neurons vulnerable. These genes were further analyzed by using mutant analysis and tissue-specific knockdown for functional validation. We found that this loss of DA neurons caused progressive locomotor dysfunction in mutants and gene knockdown analysis. The identification of genes associated with the progressive loss of DA neurons should help to uncover factors that render these neurons vulnerable in PD, and possibly develop strategies to make these neurons more resilient.


PLoS Genetics ◽  
2016 ◽  
Vol 12 (1) ◽  
pp. e1005616 ◽  
Author(s):  
Sibylle Chantal Vonesch ◽  
David Lamparter ◽  
Trudy F. C. Mackay ◽  
Sven Bergmann ◽  
Ernst Hafen

2004 ◽  
Vol 11 (6) ◽  
pp. 558-566 ◽  
Author(s):  
Jan Rehwinkel ◽  
Andrea Herold ◽  
Kerstin Gari ◽  
Thomas Köcher ◽  
Michaela Rode ◽  
...  

2019 ◽  
Author(s):  
Daniel K. Fabian ◽  
Handan Melike Dönertaş ◽  
Matías Fuentealba ◽  
Linda Partridge ◽  
Janet M. Thornton

ABSTRACTTransposable elements (TEs) inflict numerous negative effects on health and fitness as they replicate by integrating into new regions of the host genome. Even though organisms employ powerful mechanisms to demobilize TEs, transposons gradually lose repression during aging. The rising TE activity causes genomic instability and was implicated in age-dependent neurodegenerative diseases, inflammation and the determination of lifespan. It is therefore conceivable that long-lived individuals have improved TE silencing mechanisms resulting in reduced TE expression relative to their shorter-lived counterparts and fewer genomic insertions. Here, we test this hypothesis by performing the first genome-wide analysis of TE insertions and expression in populations of Drosophila melanogaster selected for longevity through late-life reproduction for 50-170 generations from four independent studies. Contrary to our expectation, TE families were generally more abundant in long-lived populations compared to non-selected controls. Although simulations showed that this was not expected under neutrality, we found little evidence for selection driving TE abundance differences. Additional RNA-seq analysis revealed a tendency for reducing TE expression in selected populations, which might be more important for lifespan than regulating genomic insertions. We further find limited evidence of parallel selection on genes related to TE regulation and transposition. However, telomeric TEs were genomically and transcriptionally more abundant in long-lived flies, suggesting improved telomere maintenance as a promising TE-mediated mechanism for prolonging lifespan. Our results provide a novel viewpoint indicating that reproduction at old age increases the opportunity of TEs to be passed on to the next generation with little impact on longevity.


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