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Cell Wall Remodeling Enzymes Modulate Fungal Cell Wall Elasticity and Osmotic Stress Resistance.

Ene IV, Walker LA, Schiavone M, Lee KK, Martin-Yken H, Dague E, Gow NA, Munro CA, Brown AJ - MBio (2015)

Bottom Line: 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.Overexpressing Crh family members in glucose-grown cells reduces cell wall elasticity, providing partial protection against hyperosmotic shock.

View Article: PubMed Central - PubMed

Affiliation: School of Medical Sciences, University of Aberdeen, Institute of Medical Sciences, Foresterhill, Aberdeen, United Kingdom.

No MeSH data available.


Related in: MedlinePlus

Genetic screen for changes in osmotic stress resistance of C. albicans strains with altered expression levels of cell wall components. C. albicans strains (see Table S1 in the supplemental material) either lacking (A) or overexpressing (B) different cell wall structural components were tested for their resistance to 2 M NaCl (1 h exposure). In panel A, relative resistance levels are expressed as the fold ratio between the osmotic stress resistance of a  mutant and that of its wild-type parental control under equivalent conditions. In panel B, the relative resistance of a tetON overexpression mutant is expressed as the ratio of the levels of osmotic stress resistance in the presence and absence of doxycycline. Boxes are colored dark green (where the mutation leads to a large increase in osmotic stress resistance) to red (where the mutation decreases osmotic stress resistance) according to the scale on the right.
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fig5: Genetic screen for changes in osmotic stress resistance of C. albicans strains with altered expression levels of cell wall components. C. albicans strains (see Table S1 in the supplemental material) either lacking (A) or overexpressing (B) different cell wall structural components were tested for their resistance to 2 M NaCl (1 h exposure). In panel A, relative resistance levels are expressed as the fold ratio between the osmotic stress resistance of a mutant and that of its wild-type parental control under equivalent conditions. In panel B, the relative resistance of a tetON overexpression mutant is expressed as the ratio of the levels of osmotic stress resistance in the presence and absence of doxycycline. Boxes are colored dark green (where the mutation leads to a large increase in osmotic stress resistance) to red (where the mutation decreases osmotic stress resistance) according to the scale on the right.

Mentions: To test this, we examined the sensitivity of various glucose- or lactate-grown C. albicans cell wall mutants to NaCl. The cells included and overexpression mutants of glucanosyltransferases (Pga4, Phr1, and Phr2), the Crh family of putative cell wall transglycosylases involved in linking chitin to β-glucan (Utr2, Crh11, and Crh12) (32), a chitin synthase (Chs3), the catalytic subunit of β-glucan synthase (Fks1), and β-glucan-linked cell wall proteins (Pir1 and Ssr1) (63–65). The inactivation of any single gene exerted relatively minor effects upon the osmotic stress resistance of glucose- and lactate-grown C. albicans cells (Fig. 5A). Interestingly, a triple crh11Δ crh12Δ utr2Δ mutation dramatically attenuated the osmotic stress resistance of lactate-grown C. albicans cells. In contrast, overexpression of CRH11, UTR2, and SSR1 increased the osmotic stress resistance of glucose-grown cells (Fig. 5B). These observations suggest that the frequency of β-glucan–chitin cross-links in the cell wall influences the osmotic stress resistance of C. albicans cells.


Cell Wall Remodeling Enzymes Modulate Fungal Cell Wall Elasticity and Osmotic Stress Resistance.

Ene IV, Walker LA, Schiavone M, Lee KK, Martin-Yken H, Dague E, Gow NA, Munro CA, Brown AJ - MBio (2015)

Genetic screen for changes in osmotic stress resistance of C. albicans strains with altered expression levels of cell wall components. C. albicans strains (see Table S1 in the supplemental material) either lacking (A) or overexpressing (B) different cell wall structural components were tested for their resistance to 2 M NaCl (1 h exposure). In panel A, relative resistance levels are expressed as the fold ratio between the osmotic stress resistance of a  mutant and that of its wild-type parental control under equivalent conditions. In panel B, the relative resistance of a tetON overexpression mutant is expressed as the ratio of the levels of osmotic stress resistance in the presence and absence of doxycycline. Boxes are colored dark green (where the mutation leads to a large increase in osmotic stress resistance) to red (where the mutation decreases osmotic stress resistance) according to the scale on the right.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4551979&req=5

fig5: Genetic screen for changes in osmotic stress resistance of C. albicans strains with altered expression levels of cell wall components. C. albicans strains (see Table S1 in the supplemental material) either lacking (A) or overexpressing (B) different cell wall structural components were tested for their resistance to 2 M NaCl (1 h exposure). In panel A, relative resistance levels are expressed as the fold ratio between the osmotic stress resistance of a mutant and that of its wild-type parental control under equivalent conditions. In panel B, the relative resistance of a tetON overexpression mutant is expressed as the ratio of the levels of osmotic stress resistance in the presence and absence of doxycycline. Boxes are colored dark green (where the mutation leads to a large increase in osmotic stress resistance) to red (where the mutation decreases osmotic stress resistance) according to the scale on the right.
Mentions: To test this, we examined the sensitivity of various glucose- or lactate-grown C. albicans cell wall mutants to NaCl. The cells included and overexpression mutants of glucanosyltransferases (Pga4, Phr1, and Phr2), the Crh family of putative cell wall transglycosylases involved in linking chitin to β-glucan (Utr2, Crh11, and Crh12) (32), a chitin synthase (Chs3), the catalytic subunit of β-glucan synthase (Fks1), and β-glucan-linked cell wall proteins (Pir1 and Ssr1) (63–65). The inactivation of any single gene exerted relatively minor effects upon the osmotic stress resistance of glucose- and lactate-grown C. albicans cells (Fig. 5A). Interestingly, a triple crh11Δ crh12Δ utr2Δ mutation dramatically attenuated the osmotic stress resistance of lactate-grown C. albicans cells. In contrast, overexpression of CRH11, UTR2, and SSR1 increased the osmotic stress resistance of glucose-grown cells (Fig. 5B). These observations suggest that the frequency of β-glucan–chitin cross-links in the cell wall influences the osmotic stress resistance of C. albicans cells.

Bottom Line: 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.Overexpressing Crh family members in glucose-grown cells reduces cell wall elasticity, providing partial protection against hyperosmotic shock.

View Article: PubMed Central - PubMed

Affiliation: School of Medical Sciences, University of Aberdeen, Institute of Medical Sciences, Foresterhill, Aberdeen, United Kingdom.

No MeSH data available.


Related in: MedlinePlus