A Key Role for the Ubiquitin Ligase UBR4 in Myofiber Hypertrophy in Drosophila and Mice.
Drosophila
HAT1
UBR4
cancer cachexia
muscle wasting
myofiber hypertrophy
myofiber size
proteolysis
skeletal muscle growth
ubiquitin ligase
Journal
Cell reports
ISSN: 2211-1247
Titre abrégé: Cell Rep
Pays: United States
ID NLM: 101573691
Informations de publication
Date de publication:
30 07 2019
30 07 2019
Historique:
received:
23
11
2018
revised:
07
05
2019
accepted:
26
06
2019
entrez:
1
8
2019
pubmed:
1
8
2019
medline:
20
8
2020
Statut:
ppublish
Résumé
Skeletal muscle cell (myofiber) atrophy is a detrimental component of aging and cancer that primarily results from muscle protein degradation via the proteasome and ubiquitin ligases. Transcriptional upregulation of some ubiquitin ligases contributes to myofiber atrophy, but little is known about the role that most other ubiquitin ligases play in this process. To address this question, we have used RNAi screening in Drosophila to identify the function of > 320 evolutionarily conserved ubiquitin ligases in myofiber size regulation in vivo. We find that whereas RNAi for some ubiquitin ligases induces myofiber atrophy, loss of others (including the N-end rule ubiquitin ligase UBR4) promotes hypertrophy. In Drosophila and mouse myofibers, loss of UBR4 induces hypertrophy via decreased ubiquitination and degradation of a core set of target proteins, including the HAT1/RBBP4/RBBP7 histone-binding complex. Together, this study defines the repertoire of ubiquitin ligases that regulate myofiber size and the role of UBR4 in myofiber hypertrophy.
Identifiants
pubmed: 31365869
pii: S2211-1247(19)30880-0
doi: 10.1016/j.celrep.2019.06.094
pmc: PMC6697171
mid: NIHMS1536139
pii:
doi:
Substances chimiques
Calmodulin-Binding Proteins
0
Drosophila Proteins
0
Muscle Proteins
0
Ubiquitin-Protein Ligases
EC 2.3.2.27
Ubr4 protein, mouse
EC 2.3.2.27
Types de publication
Journal Article
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
1268-1281.e6Subventions
Organisme : NIA NIH HHS
ID : R01 AG055532
Pays : United States
Organisme : NIAMS NIH HHS
ID : U54 AR052646
Pays : United States
Organisme : NCI NIH HHS
ID : P30 CA021765
Pays : United States
Organisme : NIA NIH HHS
ID : R01 AG047928
Pays : United States
Informations de copyright
Copyright © 2019 The Author(s). Published by Elsevier Inc. All rights reserved.
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