CRE1Crithidia Retrotransposable Element 1 (enzyme)
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They are the positive regulators XYR1, ACEII, ACEIII, LAE1, VEL1, BglR, and the HAP2/3/5 complex, as well the repressors ACEI, RCE1, and CRE1 (Figure 4).
Among the negative regulators of cellulase gene transcription, the main transcription factor is the CRE1 catabolic repressor [75].
Expression of several genes encoding transcription factors was also under regulation of XYR1 and CRE1. During cultivation in cellulose and glucose, 14 transcription factors were targeted by the CRE1-mediated mechanism of carbon catabolic repression (CCR) [45].
This last gene was a target of CCR by CRE1 under cellulose condition [45].
A study of Zou and coworkers also showed that the CRE1 binding motifs in the promoter region of cbh1 were replaced by the binding motifs of the positive regulators ACEII and the HAP2/3/5 complex, thus improving the promoter efficiency [91].
reesei as well as activates the XYR1 and CRE1 expressions [117].
A deep analysis of gene expression in two functional mutant strains of main transcription factors (XYR1 and CRE1) [35, 44, 45] and two MAPK-encoding genes showed that different signaling pathways and regulatory mechanisms are involved with the regulation of cellulase expression [43].
Here, we compared the expression patterns of signaling pathway-encoding genes in two functional mutant strains of the XYR1 positive and CRE1 negative regulators of cellulase expression in T.
[113] showed that the casein kinase pathway governs chitinase expression, and beyond that, casein kinase-dependent phosphorylation has been suggested to be an important mechanism of regulation of DNA-binding zinc finger proteins, such as CRE1 [122].
Finally, the deletion of cre1 promoted a decrease of 2.3-fold in the expression of regulatory protein velvet 1 (ID 122284).
reesei Rut-C30, which implies its direct or indirect interactions with Cre1 in T.
The two transcription regulators involved in N metabolism, nmrA-like and areA, were also analyzed and the same expression mode was detected (Table 2), suggesting that complex posttranslational regulation, such as phosphorylation on Cre1 [83], acted on these transcription regulators when T.