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Eukaryotic Cell, December 2006, p. 2128-2137, Vol. 5, No. 12
1535-9778/06/$08.00+0     doi:10.1128/EC.00211-06
Copyright © 2006, American Society for Microbiology. All Rights Reserved.

Xyr1 (Xylanase Regulator 1) Regulates both the Hydrolytic Enzyme System and D-Xylose Metabolism in Hypocrea jecorina{triangledown} ,{dagger}

Astrid R. Stricker, Karin Grosstessner-Hain,§ Elisabeth Würleitner, and Robert L. Mach*

Gene Technology, Gene Technology and Applied Biochemistry, Institute of Chemical Engineering, TU Wien, Getreidemarkt 9/166/5/2, A-1060 Wien, Austria

Received 4 July 2006/ Accepted 11 October 2006

Xyr1 (xylanase regulator 1) of the ascomycete Hypocrea jecorina (anamorph Trichoderma reesei) was recently demonstrated to play an essential role in the transcriptional regulation of the xyn1 (xylanase 1-encoding) gene expression. Consequently, this study reports on the deletion of the xyr1 gene from the H. jecorina genome. Comparative studies of the growth behavior of the different mutant strains (deleted and retransformed xyr1) grown on various carbon sources pointed to the strongly reduced ability of the xyr1 deletion strain to utilize D-xylose and xylan. Transcriptional analysis of the xyl1 (D-xylose reductase 1-encoding) gene as well as measurements of corresponding enzymatic activities gave evidence that Xyr1 takes part in the control of the fungal D-xylose pathway, in particular in the regulation of D-xylose reductase. It could be demonstrated that the uptake of D-xylose into the fungal cell is uninfluenced in the {Delta}xyr1 strain. Furthermore, transcriptional regulation of the major hydrolytic enzyme-encoding genes xyn1 and xyn2 (xylanases 1 and 2), cbh1 and cbh2 (cellobiohydrolases 1 and 2), and egl1 (endoglucanase 1) is strictly dependent on Xyr1. Regulation of the respective genes via Xyr1 is not affected by the substances mediating induction (xylose, xylobiose, and sophorose) and is indispensable for all modes of gene expression (basal, derepressed, and induced). Moreover, Xyr1, it was revealed, activated transcriptional regulation of inducer-providing enzymes such as ß-xylosidase BXLI and ß-glucosidase BGLI but was not shown to be involved in the regulation of BGLII.


* Corresponding author. Mailing address: Gene Technology, Gene Technology and Applied Biochemistry, Institute of Chemical Engineering, TU Wien, Getreidemarkt 9/166/5/2, A-1060 Wien, Austria. Phone: 43 1 58801 17251. Fax: 43 1 581 6266. E-mail: rmach{at}mail.zserv.tuwien.ac.at.

{triangledown} Published ahead of print on 20 October 2006.

{dagger} Supplemental material for this article may be found at http://ec.asm.org/.

§ Present address: Institute of Molecular Pathology, Dr.-Bohr-Gasse 7, A-1030 Wien, Austria.


Eukaryotic Cell, December 2006, p. 2128-2137, Vol. 5, No. 12
1535-9778/06/$08.00+0     doi:10.1128/EC.00211-06
Copyright © 2006, American Society for Microbiology. All Rights Reserved.







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