Evidence map›Paper›PMID 28045997›Full record

ArticlePloS one2017

Loss of BOSS Causes Shortened Lifespan with Mitochondrial Dysfunction in Drosophila.

Ayako Kohyama-Koganeya, Mizuki Kurosawa, Yoshio Hirabayashi

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
0.5field-weighted citation impact, top 39% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

4 citing papers in PubMed, 8 citations in OpenAlex.

  1. Review
  2. Review
  3. Loss ofFrontiers in cellular neuroscience · 2019
    Article
  4. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

3 authors at 1 institution in 1 country.

Ayako Kohyama-KoganeyaMolecular Membrane Neuroscience, Brain Science Institute, RIKEN, Wako-shi, Saitama, Japan.
Mizuki KurosawaMolecular Membrane Neuroscience, Brain Science Institute, RIKEN, Wako-shi, Saitama, Japan.
Yoshio HirabayashiMolecular Membrane Neuroscience, Brain Science Institute, RIKEN, Wako-shi, Saitama, Japan.
RIKEN Center for Brain Science · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Aging is a universal process that causes deterioration in biological functions of an organism over its lifetime. There are many risk factors that are thought to contribute to aging rate, with disruption of metabolic homeostasis being one of the main factors that accelerates aging. Previously, we identified a new function for the putative G-protein-coupled receptor, Bride of sevenless (BOSS), in energy metabolism. Since maintaining metabolic homeostasis is a critical factor in aging, we investigated whether BOSS plays a role in the aging process. Here, we show that BOSS affects lifespan regulation. boss null mutants exhibit shortened lifespans, and their locomotor performance and gut lipase activity-two age-sensitive markers-are diminished and similar to those of aged control flies. Reactive oxygen species (ROS) production is also elevated in boss null mutants, and their ROS defense system is impaired. The accumulation of protein adducts (advanced lipoxidation end products [ALEs] and advanced glycation end products [AGEs]) caused by oxidative stress are elevated in boss mutant flies. Furthermore, boss mutant flies are sensitive to oxidative stress challenges, leading to shortened lives under oxidative stress conditions. Expression of superoxide dismutase 2 (SOD2), which is located in mitochondria and normally regulates ROS removal, was decreased in boss mutant flies. Systemic overexpression of SOD2 rescued boss mutant phenotypes. Finally, we observed that mitochondrial mass was greater in boss mutant flies. These results suggest that BOSS affects lifespan by modulating the expression of a set of genes related to oxidative stress resistance and mitochondrial homeostasis.

Indexed as

LongevityAgingAnimalsDrosophila melanogasterDrosophila ProteinsEnergy MetabolismEye ProteinsFemaleGlycation End Products, AdvancedHomeostasisMaleMembrane GlycoproteinsMitochondriaMutationOxidative StressReactive Oxygen Speciesboss protein, DrosophilaDrosophila ProteinsEye ProteinsGlycation End Products, AdvancedMembrane GlycoproteinsReactive Oxygen SpeciesReceptors, PeptideSuperoxide DismutaseSuperoxide Dismutase 2

Identifiers

PMID28045997
PMCPMC5207625
OpenAlexW2570016523

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.