Apr 9, 2020

Introduction of the Aspergillus fumigatus α-1,2-mannosidase MsdS into Trichoderma reesei leads to abnormal polarity and improves the ligno-cellulose degradation

BioRxiv : the Preprint Server for Biology
P. Sharma GhimireCheng Jin


a-1,2-Mannosidase is an important enzyme essential for N-glycan processing and plays a significant role in the biosynthesis and organization of fungal cell wall. Lacking of -1,2-mannosidase leads to cell wall defect in yeast and filamentous fungi. Trichoderma reesei is known to be non-toxic to human, and its N-glycan on secreted glycoprotein is Man8GlcNAc2. To evaluate the significance of the N-glycan processing in T. reesei, in this study Aspergillus fumigatus -1, 2-mannosidase MsdS, an enzyme that cleaves N-linked Man8GlcNAc2 in Golgi to produce Man6GlcNAc2 on secreted glycoprotein, was introduced into T. reesei. The msdS-expressing strain Tr-MsdS produced a major glycoform of Man6GlcNAc2 on its secreted glycoproteins, instead of Man8GlcNAc2 in the parent strain. Although the cell wall content of msdS-expressing strain Tr-MsdS was changed, it appeared that the cell wall integrity was not affected. However, phenotypes such as increased conidiation, multiple budding and random branching were observed in strain Tr-MsdS. In addition, expression of MsdS into T. ressei also affected protein secretion and improved the ligno-cellulose degradation of T. reesei. Our results indicate that processing of the N-glycan is species-specific a...Continue Reading

  • References
  • Citations


  • We're still populating references for this paper, please check back later.
  • References
  • Citations


  • This paper may not have been cited yet.

Mentioned in this Paper

Haploid Cell
Wheat middlings extract
Population Group

Related Feeds

BioRxiv & MedRxiv Preprints

BioRxiv and MedRxiv are the preprint servers for biology and health sciences respectively, operated by Cold Spring Harbor Laboratory. Here are the latest preprint articles (which are not peer-reviewed) from BioRxiv and MedRxiv.