Trichoderma reesei XYR1 recruits SWI/SNF to facilitate cellulase gene expression
Summary Cellulase gene expression in Trichoderma reesei is highly responsive to environmental cues and is under stringent regulation by multiple transcription factors. XYR1 (Xylanase regulator 1) has been identified as the most important transcriptional activator of cellulase/hemicellulase gene expr...
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Veröffentlicht in: | Molecular microbiology 2019-10, Vol.112 (4), p.1145-1162 |
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Zusammenfassung: | Summary
Cellulase gene expression in Trichoderma reesei is highly responsive to environmental cues and is under stringent regulation by multiple transcription factors. XYR1 (Xylanase regulator 1) has been identified as the most important transcriptional activator of cellulase/hemicellulase gene expression although the precise transactivating mechanism remains largely elusive. Here we show that the activation domain of XYR1 interacts with the T. reesei homolog of the TrSNF12 subunit of SWI/SNF complex. Deletion of Trsnf12 markedly impaired the induced cellulase gene expression. Individual loss of other SWI/SNF subunits including the catalytic subunit also severely compromised cellulase gene expression and interfered with loss of histone H4 in the cbh1 and eg1 promoters upon cellulose induction. In addition, we find that the SWI/SNF occupancy on cellulase gene promoters strictly required XYR1 and TrSNF12 but TrSNF12 was dispensable for the XYR1 binding to these promoters. These data suggest a model in which XYR1 recruits SWI/SNF through direct interactions with TrSNF12 to remodel chromatin at cellulase gene promoters, thereby activating cellulase gene expression to initiate the cellulolytic response in T. reesei.
The mechanism by which the key transcriptional activator XYR1 activates cellulase gene expression in Trichoderma reesei remains largely unknown. We show that XYR1 interacts with the SWI/SNF homologous subunit TrSNF12 and potentially recruits this chromatin remodeling complex to alter the relevant chromatin environment, which then contribute to the induced cellulase gene expression. |
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ISSN: | 0950-382X 1365-2958 |
DOI: | 10.1111/mmi.14352 |