Background: The hypercellulolytic mutant Hypocrea jecorina (anamorph Trichoderma reesei) RUT C30 is the H. jecorina strain most frequently used for cellulase fermentations and has also often been employed for basic research on cellulase regulation. This strain has been reported to contain a truncated carbon catabolite repressor gene cre1 and is consequently carbon catabolite derepressed. To date this and an additional frame-shift mutation in the glycoprotein-processing βglucosidase II encoding gene are the only known genetic differences in strain RUT C30. Results: In the present paper we show that H. jecorina RUT C30 lacks an 85 kb genomic fragment, and consequently misses additional 29 genes comprising transcription factors, enzymes of the primary metabolism and transport proteins. This loss is already present in the ancestor of RUT C30 – NG 14 – and seems to have occurred in a palindromic AT-rich repeat (PATRR) typically inducing chromosomal translocations, and is not linked to the cre1 locus. The mutation of the cre1 locus has specifically occurred in RUT C30. Some of the genes that are lacking in RUT C30 could be correlated with pronounced alterations in its phenotype, such as poor growth on α-linked oligoand polyglucosides (loss of maltose permease), or disturbance of osmotic homeostasis. Conclusion: Our data place a general caveat on the use of H. jecorina RUT C30 for further basic research.
@article{osti_1626467,
author = {Seidl, Verena and Gamauf, Christian and Druzhinina, Irina S. and Seiboth, Bernhard and Hartl, Lukas and Kubicek, Christian P.},
title = {The <em>Hypocrea jecorina (Trichoderma reesei)</em> hypercellulolytic mutant RUT C30 lacks a 85 kb (29 gene-encoding) region of the wild-type genome},
annote = {Background: The hypercellulolytic mutant Hypocrea jecorina (anamorph Trichoderma reesei) RUT C30 is the H. jecorina strain most frequently used for cellulase fermentations and has also often been employed for basic research on cellulase regulation. This strain has been reported to contain a truncated carbon catabolite repressor gene cre1 and is consequently carbon catabolite derepressed. To date this and an additional frame-shift mutation in the glycoprotein-processing βglucosidase II encoding gene are the only known genetic differences in strain RUT C30. Results: In the present paper we show that H. jecorina RUT C30 lacks an 85 kb genomic fragment, and consequently misses additional 29 genes comprising transcription factors, enzymes of the primary metabolism and transport proteins. This loss is already present in the ancestor of RUT C30 – NG 14 – and seems to have occurred in a palindromic AT-rich repeat (PATRR) typically inducing chromosomal translocations, and is not linked to the cre1 locus. The mutation of the cre1 locus has specifically occurred in RUT C30. Some of the genes that are lacking in RUT C30 could be correlated with pronounced alterations in its phenotype, such as poor growth on α-linked oligoand polyglucosides (loss of maltose permease), or disturbance of osmotic homeostasis. Conclusion: Our data place a general caveat on the use of H. jecorina RUT C30 for further basic research.},
doi = {10.1186/1471-2164-9-327},
url = {https://www.osti.gov/biblio/1626467},
journal = {BMC Genomics},
issn = {ISSN 1471-2164},
number = {1},
volume = {9},
place = {United States},
publisher = {Springer},
year = {2008},
month = {07}}