Document Detail


Reactive oxygen species can modulate circadian phase and period in Neurospora crassa.
MedLine Citation:
PMID:  23277144     Owner:  NLM     Status:  Publisher    
Abstract/OtherAbstract:
Reactive oxygen species may serve as signals coupling metabolism to other cell functions. Beside being byproducts of normal metabolism, they are generated at elevated levels under environmental stress situations. We analyzed how reactive oxygen species affect the circadian clock in the model organism Neurospora crassa. In light-dark cycles, an increase in the levels of reactive oxygen species advanced the phase of both the conidiation rhythm and the expression of the clock gene frequency. Our results indicate a dominant role of the superoxide anion in the control of the phase. Elevation of superoxide production resulted in the activation of protein phosphatase 2A, a regulator of the positive element of the circadian clock. Our data indicate that even under non-stress conditions, reactive oxygen species affect circadian timekeeping. Reduction of their basal levels results in delay of the phase in light-dark cycles and a longer period under constant conditions. We show that under entrained conditions the phase depends on the temperature and reactive oxygen species contribute to this effect. Our results suggest that the superoxide anion is an important factor controlling the circadian oscillator, and is able to reset the clock most probably by activating protein phosphatase 2A, thereby modulating the activity of the White Collar Complex.
Authors:
Norbert Gyöngyösi; Dóra Nagy; Krisztina Makara; Krisztina Ella; Krisztina Káldi
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Publication Detail:
Type:  JOURNAL ARTICLE     Date:  2012-12-28
Journal Detail:
Title:  Free radical biology & medicine     Volume:  -     ISSN:  1873-4596     ISO Abbreviation:  Free Radic. Biol. Med.     Publication Date:  2012 Dec 
Date Detail:
Created Date:  2013-1-1     Completed Date:  -     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  8709159     Medline TA:  Free Radic Biol Med     Country:  -    
Other Details:
Languages:  ENG     Pagination:  -     Citation Subset:  -    
Copyright Information:
Copyright © 2012. Published by Elsevier Inc.
Affiliation:
Department of Physiology, Semmelweis University, Tűzoltó u. 37-47, Hungary, H-1092.
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