Document Detail

The induction of autophagy by mechanical stress.
MedLine Citation:
PMID:  22024750     Owner:  NLM     Status:  MEDLINE    
The ability to respond and adapt to changes in the physical environment is a universal and essential cellular property. Here we demonstrated that cells respond to mechanical compressive stress by rapidly inducing autophagosome formation. We measured this response in both Dictyostelium and mammalian cells, indicating that this is an evolutionarily conserved, general response to mechanical stress. In Dictyostelium, the number of autophagosomes increased 20-fold within 10 min of 1 kPa pressure being applied and a similar response was seen in mammalian cells after 30 min. We showed in both cell types that autophagy is highly sensitive to changes in mechanical pressure and the response is graduated, with half-maximal responses at ~0.2 kPa, similar to other mechano-sensitive responses. We further showed that the mechanical induction of autophagy is TOR-independent and transient, lasting until the cells adapt to their new environment and recover their shape. The autophagic response is therefore part of an integrated response to mechanical challenge, allowing cells to cope with a continuously changing physical environment.
Jason S King; Douwe M Veltman; Robert H Insall
Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Autophagy     Volume:  7     ISSN:  1554-8635     ISO Abbreviation:  Autophagy     Publication Date:  2011 Dec 
Date Detail:
Created Date:  2012-04-02     Completed Date:  2012-06-18     Revised Date:  2013-06-27    
Medline Journal Info:
Nlm Unique ID:  101265188     Medline TA:  Autophagy     Country:  United States    
Other Details:
Languages:  eng     Pagination:  1490-9     Citation Subset:  IM    
Beatson Institute for Cancer Research, Glasgow, Scotland, UK.
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MeSH Terms
Adaptation, Physiological
Cell Line, Tumor
Dictyostelium / cytology*,  physiology
Phagosomes / metabolism
Stress, Mechanical*
TOR Serine-Threonine Kinases / metabolism
Grant Support
//Cancer Research UK
Reg. No./Substance:
EC Serine-Threonine Kinases

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine

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