DEMONSTRATION OF A FIBRILLAR COMPONENT IN THE CELL WALL OF THE YEAST SACCHAROMYCES CEREVISIAE AND ITS CHEMICAL NATURE

Abstract

The ultrastructure of isolated cell walls of Saccharomyces cerevisiae from the log and stationary phases of growth was studied after treatment with the following enzymes: purified endo-3-(1 -~ 3)-glucanase and endo-3-(l -~ 6)-glucanase produced by Bacillus circulans; purified exo-3-glucanase and endo-3-(1 ~ 3)-glucanase produced by Schizosaccharomyces versatilis; commercial Pronase. While exo-3-glucanase from S. versatilis had no electron microscopically detectable effect on the walls, Pronase removed part of the external amorphous wall material disclosing an amorphous wall layer in which fibrils were indistinctly visible. Amorphous wall material was completely removed by the effect of either endo-3-(l -~ 3)-or endo-3-(l ~ 6)-glucanase of B. circulans or by a mixture of the two enzymes. As a result of these treatments a continuous fibrillar component appeared, composed of densely interwoven microfibrils resisting further action by both of the B. circulans enzymes. The fibrillar wall component was also demonstrated in untreated cell walls by electron microscopy after negative staining. Because of the complete disappearance of the fibrils following treatment with the S. versatilis endo-3-(1 -~ 3)-glucanase it can be concluded that this fibrillar component is composed of 3-(1 --* 3)-linked glucan. Bud scars were the only wall structures resistant to the effect of the latter enzyme.

Effects of the F-actin inhibitor latrunculin A on the budding yeast Saccharomyces cerevisiae

“…5d-f), which differed from the WT cell walls isolated by cell disruption using ballotini. The WT cells retained their ovoid shape (Kopecká et al, 1974). This indicated that the rigidity of the cell walls in the LA-inhibited cells had been affected.…”

“…2f) and buds ( Fig. 2g) of b-1,3-glucan microfibrils (Kopecká et al, 1974). A few cell wall ridges and plasma membrane invaginations ( Fig.…”

“…Our reinvestigation of the phenotypes of act1-1 and act1-2 mutant cells at 37 uC proved that AC are necessary for the correct spatial positioning and orientation of secretory pathways to the bud and septum, and for vectorial movement of the SV along the AC ; act1-1 cells at 23 uC have 'faint actin cables' that delay bud formation, bud growth and nuclear migration to the bud neck, in contrast to nuclear division Kopecká & Yamaguchi, 2011). This indicated the existence of two cytoskeleton-dependent pathways: (i) the 'actin pathway' for bud formation, bud growth and nuclear migration, and (ii) the 'microtubule pathway' for nuclear division (Kopecká & Yamaguchi, 2011) that may correspond to the two cell-cycle pathways identified by CDC mutants (Hartwell et al, 1974 Klis et al, 2014) that under examination with electron microscopy have an amorphous appearance (Kopecká et al, 1974).…”

Compounds active against cell walls of medically important fungi

“…The innermost layer is predominantly composed of microfibrils of beta-(1,3)-glucan with some beta-(1,6) branch points (143,152,153), while the outer layer is essentially all mannoprotein (9,104). In contrast to the cell walls of most medically important fungi, the cell wall of S. cerevisiae is relatively poor in chitin and depends on the beta-(1,3)-glucan for maintenance of its structural integrity (148).…”

Cell surface structures in osmotically fragile mutants of Saccharomyces cerevisiae

“…Microfibrils of p-(1+3)-glucan make up the wall fibrillar skeleton (Kopecki et al, 1974;.Houwink & Kreger, 1953), which is masked with amorphous P-glucans (Kopecka et al, 1974) and mannoproteins (cf. Bacon, 1981;Kopecka, 1985).…”