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Biological Chemistry

Editor-in-Chief: Brüne, Bernhard

Editorial Board: Buchner, Johannes / Lei, Ming / Ludwig, Stephan / Thomas, Douglas D. / Turk, Boris / Wittinghofer, Alfred

IMPACT FACTOR 2018: 3.014
5-year IMPACT FACTOR: 3.162

CiteScore 2018: 3.09

SCImago Journal Rank (SJR) 2018: 1.482
Source Normalized Impact per Paper (SNIP) 2018: 0.820

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Volume 383, Issue 3-4


Neurospora crassa Catalases, Singlet Oxygen and Cell Differentiation

L. Peraza / W. Hansberg
Published Online: 2005-06-01 | DOI: https://doi.org/10.1515/BC.2002.058


The morphogenetic transitions of the N. crassa asexual life cycle are responses to a hyperoxidant state in which probably singlet oxygen is generated. Induction of catalase activity and catalase oxidation by singlet oxygen are consequences of this recurrent hyperoxidant state. Here the biochemical properties and regulation of two large monofunctional catalases are reviewed, and a new catalaseperoxidase gene and activity is described. Catalase-3 is associated to growing and Catalase-1 to nongrowing cells. Under stressful conditions one of these catalases is synthesized, depending on whether growth can be continued or a resistant cell has to be made. The catalaseperoxidase Catalase-2 was possibly derived from a bacterial enzyme. In contrast to the other catalases, Catalase-2 had catalase and peroxidase activity. Catalase-2 was expressed under conditions in which vacuolization of hyphae is observed. All three enzymes have a chlorin in its active site instead of ferroprotoheme IX and are resistant to molar concentrations of hydrogen peroxide. These and all other catalases tested so far are oxidized by singlet oxygen, probably at the heme moiety. The catalase activity is virtually unaffected by oxidation, but the enzymes are probably degraded more rapidly than the unmodified ones.

About the article

Published Online: 2005-06-01

Published in Print: 2002-04-12

Citation Information: Biological Chemistry, Volume 383, Issue 3-4, Pages 569–575, ISSN (Print) 1431-6730, DOI: https://doi.org/10.1515/BC.2002.058.

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