Does overexpression of Cu,Zn-SOD extend life span in Drosophila melanogaster?

2003 ◽  
Vol 38 (3) ◽  
pp. 227-230 ◽  
Author(s):  
W Orr
Keyword(s):  
Drosophila Melanogaster ◽  
Life Span ◽  
Extend Life Span

scholarly journals The genetic paradigms of dietary restriction fail to extend life span in cep-1(gk138) mutant of C. elegans p53 due to possible background mutations

2020 ◽  
Author(s):  
Anita Goyala ◽  
Aiswarya Baruah ◽  
Arnab Mukhopadhyay
Keyword(s):  
Life Span ◽  
Dietary Restriction ◽  
Model Systems ◽  
Regulation Of Expression ◽  
Life Span Extension ◽  
Phenotypic Differences ◽  
C Elegans ◽  
Xenobiotic Detoxification ◽  
Organismal Biology ◽  
Extend Life Span

AbstractDietary restriction (DR) increases life span and improves health in most model systems tested, including non-human primates. In C. elegans, as in other models, DR leads to reprogramming of metabolism, improvements in mitochondrial health, large changes in gene expression, including increase in expression of cytoprotective genes, better proteostasis etc. Understandably, multiple global transcriptional regulators like transcription factors FOXO/DAF-16, FOXA/PHA-4, HSF1/HSF-1 and NRF2/SKN-1 are important for DR longevity. Considering the wide-ranging effects of p53 on organismal biology, we asked whether the C. elegans ortholog, CEP-1 is required for DR-mediated longevity assurance. We employed the widely-used TJ1 strain of cep-1(gk138). We show that cep-1(gk138) suppresses the life span extension of two genetic paradigms of DR, but two non-genetic modes of DR remain unaffected in this strain. We find that in cep-1(gk138), two aspects of DR, increased autophagy and the up-regulation of expression of cytoprotective xenobiotic detoxification program (cXDP) genes are dampened. Importantly, we find that background mutation(s) in the strain may be the actual cause for the phenotypic differences that we observed and cep-1 may not be directly involved in genetic DR-mediated longevity assurance in worms. Identifying these mutation(s) may reveal a novel regulator of longevity required specifically by genetic modes of DR.

scholarly journals Genetic and pharmacological interventions in the aging motor nervous system slow motor aging and extend life span inC. elegans

2019 ◽  
Vol 5 (1) ◽  
pp. eaau5041 ◽  
Author(s):  
Guang Li ◽  
Jianke Gong ◽  
Jie Liu ◽  
Jinzhi Liu ◽  
Huahua Li ◽  
...  
Keyword(s):  
Nervous System ◽  
Life Span ◽  
Motor Neurons ◽  
Neuromuscular Junctions ◽  
Functional Decline ◽  
Bk Channel ◽  
Pharmacological Interventions ◽  
Genetic Ablation ◽  
Extend Life Span ◽  
Age Dependent

As animals and humans age, the motor system undergoes a progressive functional decline, leading to frailty. Age-dependent functional deteriorations at neuromuscular junctions (NMJs) contribute to this motor aging. However, it is unclear whether one can intervene in this process to slow motor aging. TheCaenorhabditis elegansBK channel SLO-1 dampens synaptic transmission at NMJs by repressing synaptic release from motor neurons. Here, we show that genetic ablation of SLO-1 not only reduces the rate of age-dependent motor activity decline to slow motor aging but also surprisingly extends life span. SLO-1 acts in motor neurons to mediate both functions. Genetic knockdown or pharmacological inhibition of SLO-1 in aged, but not young, worms can slow motor aging and prolong longevity. Our results demonstrate that genetic and pharmacological interventions in the aging motor nervous system can promote both health span and life span.

scholarly journals Neuronal Expression of p53 Dominant-Negative Proteins in Adult Drosophila melanogaster Extends Life Span

2005 ◽  
Vol 15 (22) ◽  
pp. 2063-2068 ◽  
Author(s):  
Johannes H. Bauer ◽  
Peter C. Poon ◽  
Heather Glatt-Deeley ◽  
John M. Abrams ◽  
Stephen L. Helfand
Keyword(s):  
Drosophila Melanogaster ◽  
Life Span ◽  
Dominant Negative ◽  
Neuronal Expression ◽  
Adult Drosophila

scholarly journals Monoassociation withLactobacillus plantarumDisrupts Intestinal Homeostasis in AdultDrosophila melanogaster

mBio ◽  
2018 ◽  
Vol 9 (4) ◽  
Author(s):  
David Fast ◽  
Aashna Duggal ◽  
Edan Foley
Keyword(s):  
Drosophila Melanogaster ◽  
Stem Cell ◽  
Simple Model ◽  
Life Span ◽  
Lactobacillus Plantarum ◽  
Adult Longevity ◽  
Intestinal Homeostasis ◽  
Content Type ◽  
Cell Divisions ◽  
Stem Cell Divisions

ABSTRACTAdultDrosophila melanogasterraised in the absence of symbiotic bacteria have fewer intestinal stem cell divisions and a longer life span than their conventionally reared counterparts. However, we do not know if increased stem cell divisions are essential for symbiont-dependent regulation of longevity. To determine if individual symbionts cause aging-dependent death inDrosophila, we examined the impacts of common symbionts on host longevity. We found that monoassociation of adultDrosophilawithLactobacillus plantarum, a widely reported fly symbiont and member of the probioticLactobacillusgenus, curtails adult longevity relative to germfree counterparts. The effects ofLactobacillus plantarumon life span were independent of intestinal aging. Instead, we found that association withLactobacillus plantarumcauses an extensive intestinal pathology within the host, characterized by loss of stem cells, impaired epithelial renewal, and a gradual erosion of epithelial ultrastructure. Our study uncovers an unknown aspect ofLactobacillus plantarum-Drosophilainteractions and establishes a simple model to characterize symbiont-dependent disruption of intestinal homeostasis.IMPORTANCEUnder homeostatic conditions, gut bacteria provide molecular signals that support the organization and function of the host intestine. Sudden shifts in the composition or distribution of gut bacterial communities impact host receipt of bacterial cues and disrupt tightly regulated homeostatic networks. We used theDrosophila melanogastermodel to determine the effects of prominent fly symbionts on host longevity and intestinal homeostasis. We found that monoassociation withLactobacillus plantarumleads to a loss of intestinal progenitor cells, impaired epithelial renewal, and disruption of gut architecture as flies age. These observations uncover a novel phenotype caused by monoassociation of a germfree host with a common symbiont and establish a simple model to characterize symbiont-dependent loss of intestinal homeostasis.

scholarly journals Specific Dietary Carbohydrates Differentially Influence the Life Span and Fecundity of Drosophila melanogaster

2013 ◽  
Vol 69 (1) ◽  
pp. 3-12 ◽  
Author(s):  
Oleh V. Lushchak ◽  
Dmytro V. Gospodaryov ◽  
Bohdana M. Rovenko ◽  
Ihor S. Yurkevych ◽  
Natalia V. Perkhulyn ◽  
...  
Keyword(s):  
Drosophila Melanogaster ◽  
Life Span ◽  
Dietary Carbohydrates

scholarly journals Chromatin-modifying genetic interventions suppress age-associated transposable element activation and extend life span in Drosophila

2016 ◽  
Vol 113 (40) ◽  
pp. 11277-11282 ◽  
Author(s):  
Jason G. Wood ◽  
Brian C. Jones ◽  
Nan Jiang ◽  
Chengyi Chang ◽  
Suzanne Hosier ◽  
...  
Keyword(s):  
Life Span ◽  
Dietary Restriction ◽  
Fat Body ◽  
Transcriptase Inhibitor ◽  
Dna Double Strand Breaks ◽  
Expression Of Genes ◽  
Age Related ◽  
Extend Life Span ◽  
Genetic Interventions ◽  
Heterochromatin Structure

Transposable elements (TEs) are mobile genetic elements, highly enriched in heterochromatin, that constitute a large percentage of the DNA content of eukaryotic genomes. Aging in Drosophila melanogaster is characterized by loss of repressive heterochromatin structure and loss of silencing of reporter genes in constitutive heterochromatin regions. Using next-generation sequencing, we found that transcripts of many genes native to heterochromatic regions and TEs increased with age in fly heads and fat bodies. A dietary restriction regimen, known to extend life span, repressed the age-related increased expression of genes located in heterochromatin, as well as TEs. We also observed a corresponding age-associated increase in TE transposition in fly fat body cells that was delayed by dietary restriction. Furthermore, we found that manipulating genes known to affect heterochromatin structure, including overexpression of Sir2, Su(var)3–9, and Dicer-2, as well as decreased expression of Adar, mitigated age-related increases in expression of TEs. Increasing expression of either Su(var)3–9 or Dicer-2 also led to an increase in life span. Mutation of Dicer-2 led to an increase in DNA double-strand breaks. Treatment with the reverse transcriptase inhibitor 3TC resulted in decreased TE transposition as well as increased life span in TE-sensitized Dicer-2 mutants. Together, these data support the retrotransposon theory of aging, which hypothesizes that epigenetically silenced TEs become deleteriously activated as cellular defense and surveillance mechanisms break down with age. Furthermore, interventions that maintain repressive heterochromatin and preserve TE silencing may prove key to preventing damage caused by TE activation and extending healthy life span.

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