Galactosylation of cell-surface glycoprotein required for hyphal growth and cell wall integrity in Schizosaccharomyces japonicus

Schizosaccharomyces japonicus is a dimorphic yeast, transiting between unicellular and hyphal growth. The glyco-proteins of fission yeast contain, in addition to mannose (Man), a large number of galactose (Gal) residues. Previously, we reported that the cell-surface O-glycans of S. japonicus comprise mainly tri-saccharides (Gal-Man-Man) as a main component, in contrast to the tetra-saccharides observed in other Schizosaccharomyces species. Here we have investi-gated the function of cell-surface Gal residues in S. japonicus. Because disruption of gms1+, encoding the UDP-Gal transporter required for galactomannan synthesis, abolishes cell-surface galactosylation in Schizosaccharomyces pombe, we constructed a deletion mutant of the homologous gene in S. japonicus gms1D [gms1 (S.j)] and determined the N- and O-linked oligosaccharide structures present on the cell surface. Disruption of gms1 (S.j) resulted in a complete lack of Gal on the cell surface, indicating that Gms1 plays an essential role in supplying UDP-Gal from the cytoplasm to the Golgi lumen. Analytical microscopy of gms1D demonstrated that the lack of cell-surface Gal did not affect cell growth or morphology during vegetative growth. However, hyphal development was blocked in gms1D, even in the presence of the topoisomerase I inhibitor camptothecin, which is known to induce hyphal differentiation in wild-type S. japonicus. Collectively, these findings show that Gal-containing oligosaccharides are required for cell wall integrity during filamentous growth in S. japonicus.(c) 2022, The Society for Biotechnology, Japan. All rights reserved.

Automated summary

Schizosaccharomyces japonicus requires Gal-containing oligosaccharides for cell wall integrity during filamentous growth. The cell-surface of S. japonicus primarily consists of tri-saccharides (Gal-Man-Man), unlike other species. Disruption of the UDP-Gal transporter gene results in a complete lack of Gal on the cell surface and blocks hyphal development.