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Vol. 19, Issue 8, 3254-3262, August 2008

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More Than a Repair Enzyme: Aspergillus nidulans Photolyase-like CryA Is a Regulator of Sexual Development

Özgür Bayram^*, Christoph Biesemann^*,, Sven Krappmann^*,, Paul Galland, and Gerhard H. Braus^*

*Institute of Microbiology and Genetics, Department of Molecular Microbiology and Genetics, Georg August University, D-37077 Göttingen, Germany; and Faculty of Biology, Philipps University, D-35032 Marburg, Germany

Submitted January 22, 2008; Revised May 6, 2008; Accepted May 9, 2008
Monitoring Editor: William P. Tansey

Cryptochromes are blue-light receptors that have presumably evolved from the DNA photolyase protein family, and the genomes of many organisms contain genes for both types of molecules. Both protein structures resemble each other, which suggests that light control and light protection share a common ancient origin. In the genome of the filamentous fungus Aspergillus nidulans, however, only one cryptochrome/photolyase-encoding gene, termed cryA, was identified. Deletion of the cryA gene triggers sexual differentiation under inappropriate culture conditions and results in up-regulation of transcripts encoding regulators of fruiting body formation. CryA is a protein whose N- and C-terminal synthetic green fluorescent protein fusions localize to the nucleus. CryA represses sexual development under UVA_{350-370 nm} light both on plates and in submerged culture. Strikingly, CryA exhibits photorepair activity as demonstrated by heterologous complementation of a DNA repair-deficient Escherichia coli strain as well as overexpression in an A. nidulans uvsB genetic background. This is in contrast to the single deletion cryA strain, which does not show increased sensitivity toward UV-induced damage. In A. nidulans, cryA encodes a novel type of cryptochrome/photolyase that exhibits a regulatory function during light-dependent development and DNA repair activity. This represents a paradigm for the evolutionary transition between photolyases and cryptochromes.

Present addresses: Max Planck Institute for Experimental Medicine, Molecular Neurobiology, Hermann Rein Strasse 3, D-37075 Göttingen, Germany;

Research Center for Infectious Diseases, Julius Maximilians University, Röntgenring 11, D-97070 Würzburg, Germany.

Address correspondence to: Gerhard H. Braus (gbraus{at}gwdg.de)

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				R. Pokorny, T. Klar, U. Hennecke, T. Carell, A. Batschauer, and L.-O. Essen Recognition and repair of UV lesions in loop structures of duplex DNA by DASH-type cryptochrome PNAS, December 30, 2008; 105(52): 21023 - 21027. [Abstract] [Full Text] [PDF]