Taxonomic group: fungi / Ascomycota
(Phylum: Ascomycota)
Organ / tissue: cell wall
NCBI PubMed ID: 26220968Publication DOI: 10.1128/mBio.00986-15Journal NLM ID: 101519231Publisher: Washington, DC: American Society for Microbiology
Correspondence: al.brown

abdn.ac.uk
Institutions: Université de Toulouse, CNRS, UMR5504, Toulouse, France, School of Medical Sciences, University of Aberdeen, Institute of Medical Sciences, Aberdeen, UK, INSA, UPS, INP, LISBP, Toulouse, France, INRA, UMR792 Ingénierie des Systèmes Biologiques et des Procédés, Toulouse, France, CNRS, LAAS, Toulouse, France, Université de Toulouse, LAAS, Toulouse, France, School of Medical Sciences, University of Aberdeen, Institute of Medical Sciences, Foresterhill, Aberdeen, United Kingdom
The fungal cell wall confers cell morphology and protection against environmental insults. For fungal pathogens, the cell wall is a key immunological modulator and an ideal therapeutic target. Yeast cell walls possess an inner matrix of interlinked β-glucan and chitin that is thought to provide tensile strength and rigidity. Yeast cells remodel their walls over time in response to environmental change, a process controlled by evolutionarily conserved stress (Hog1) and cell integrity (Mkc1, Cek1) signaling pathways. These mitogen-activated protein kinase (MAPK) pathways modulate cell wall gene expression, leading to the construction of a new, modified cell wall. We show that the cell wall is not rigid but elastic, displaying rapid structural realignments that impact survival following osmotic shock. Lactate-grown Candida albicans cells are more resistant to hyperosmotic shock than glucose-grown cells. We show that this elevated resistance is not dependent on Hog1 or Mkc1 signaling and that most cell death occurs within 10 min of osmotic shock. Sudden decreases in cell volume drive rapid increases in cell wall thickness. The elevated stress resistance of lactate-grown cells correlates with reduced cell wall elasticity, reflected in slower changes in cell volume following hyperosmotic shock. The cell wall elasticity of lactate-grown cells is increased by a triple mutation that inactivates the Crh family of cell wall cross-linking enzymes, leading to increased sensitivity to hyperosmotic shock. Overexpressing Crh family members in glucose-grown cells reduces cell wall elasticity, providing partial protection against hyperosmotic shock. These changes correlate with structural realignment of the cell wall and with the ability of cells to withstand osmotic shock.
cell wall, glycosyltransferases, Microscopy
Structure type: structural motif or average structure
Location inside paper: p. 1, column 2, paragraph 1
Trivial name: chitin
Compound class: cell wall polysaccharide, glucan, cell wall polisaccharide
Contained glycoepitopes: IEDB_135813,IEDB_137340,IEDB_141807,IEDB_151531,IEDB_153212,IEDB_241099,IEDB_423114,IEDB_423150,SB_74,SB_85
Methods: AFM, HPF-TEM
Comments, role: important for rigidity and physical strength of the cell wall; composes 1-3% of the cell wall; covalently cross-lilnked to the b-glucan network
Related record ID(s): 42362, 48507
NCBI Taxonomy refs (TaxIDs): 5476Reference(s) to other database(s): GTC:G97099AY
Show glycosyltransferases
There is only one chemically distinct structure: