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

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 ide...

Full description

Bibliographic Details
Main Authors: Ayako Kohyama-Koganeya, Mizuki Kurosawa, Yoshio Hirabayashi
Format: Article
Language:English
Published: Public Library of Science (PLoS) 2017-01-01
Series:PLoS ONE
Online Access:http://europepmc.org/articles/PMC5207625?pdf=render
_version_ 1818944855248732160
author Ayako Kohyama-Koganeya
Mizuki Kurosawa
Yoshio Hirabayashi
author_facet Ayako Kohyama-Koganeya
Mizuki Kurosawa
Yoshio Hirabayashi
author_sort Ayako Kohyama-Koganeya
collection DOAJ
description 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.
first_indexed 2024-12-20T07:49:51Z
format Article
id doaj.art-9ceec48c716c4993931b4ad06bdf5f53
institution Directory Open Access Journal
issn 1932-6203
language English
last_indexed 2024-12-20T07:49:51Z
publishDate 2017-01-01
publisher Public Library of Science (PLoS)
record_format Article
series PLoS ONE
spelling doaj.art-9ceec48c716c4993931b4ad06bdf5f532022-12-21T19:47:52ZengPublic Library of Science (PLoS)PLoS ONE1932-62032017-01-01121e016907310.1371/journal.pone.0169073Loss of BOSS Causes Shortened Lifespan with Mitochondrial Dysfunction in Drosophila.Ayako Kohyama-KoganeyaMizuki KurosawaYoshio HirabayashiAging 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.http://europepmc.org/articles/PMC5207625?pdf=render
spellingShingle Ayako Kohyama-Koganeya
Mizuki Kurosawa
Yoshio Hirabayashi
Loss of BOSS Causes Shortened Lifespan with Mitochondrial Dysfunction in Drosophila.
PLoS ONE
title Loss of BOSS Causes Shortened Lifespan with Mitochondrial Dysfunction in Drosophila.
title_full Loss of BOSS Causes Shortened Lifespan with Mitochondrial Dysfunction in Drosophila.
title_fullStr Loss of BOSS Causes Shortened Lifespan with Mitochondrial Dysfunction in Drosophila.
title_full_unstemmed Loss of BOSS Causes Shortened Lifespan with Mitochondrial Dysfunction in Drosophila.
title_short Loss of BOSS Causes Shortened Lifespan with Mitochondrial Dysfunction in Drosophila.
title_sort loss of boss causes shortened lifespan with mitochondrial dysfunction in drosophila
url http://europepmc.org/articles/PMC5207625?pdf=render
work_keys_str_mv AT ayakokohyamakoganeya lossofbosscausesshortenedlifespanwithmitochondrialdysfunctionindrosophila
AT mizukikurosawa lossofbosscausesshortenedlifespanwithmitochondrialdysfunctionindrosophila
AT yoshiohirabayashi lossofbosscausesshortenedlifespanwithmitochondrialdysfunctionindrosophila