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Disruption of non-anchored cell wall protein NCW-1 promotes cellulase production by increasing cellobiose uptake in Neurospora crassa

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Abstract

Objectives

To elucidate the mechanism of cellulase signal transduction in filamentous fungi including the components of the cellulase induction pathway.

Results

Neurospora crassa ncw-1 encodes a non-anchored cell wall protein. The absence of ncw-1 increased cellulase gene expression and this is not due to relieving carbon catabolite repression mediated by the cre-1 pathway. A mutant lacking genes encoding both three major β-glucosidase enzymes and NCW-1 (Δ3βGΔncw-1) was constructed. Transcriptome analysis of the quadruple mutant demonstrated enhanced expression of cellodextrin transporters after ncw-1 deletion, indicating that ncw-1 affects cellulase expression and production by inhibiting the uptake of the cellodextrin.

Conclusions

NCW-1 is a novel component that plays a critical role in the cellulase induction signaling pathway.

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Acknowledgements

We thank Dr. Raymond J St. Leger from University of Maryland, College Park for revising the manuscript. This work was supported by the National Natural Science Foundation of China (31501007, 31471186) and Tianjin Zhuanxiang Grant 11ZCZDSY08400.

Supporting information

Supplementary Table 1—Primers used in this study.

Supplementary Table 2—Relative expression level of all genes detected in Δ3βG and Δ3βGΔncw-1 on 1 % (w/v) cellobiose.

Supplementary Fig. 1—Hyphal morphologies of Δncw-1 and wild type strains.

Supplementary Fig. 2—The expression levels of cellulase genes and transcriptional factor cre-1 in Δncw-1 strain monitored by quantitative RT-PCR after grown on Avicel for 2 days.

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Correspondence to Chaoguang Tian.

Additional information

Liangcai Lin and Yong Chen have contributed equally to this work.

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Supplementary material 2 (DOCX 462 kb)

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Lin, L., Chen, Y., Li, J. et al. Disruption of non-anchored cell wall protein NCW-1 promotes cellulase production by increasing cellobiose uptake in Neurospora crassa . Biotechnol Lett 39, 545–551 (2017). https://doi.org/10.1007/s10529-016-2274-1

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  • DOI: https://doi.org/10.1007/s10529-016-2274-1

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