Lagorce, Arnaud;
Le Berre‐Anton, Veronique;
Aguilar‐Uscanga, Blanca;
Martin‐Yken, Helene;
Dagkessamanskaia, Adilia;
François, Jean
Involvement of GFA1, which encodes glutamine–fructose‐6‐phosphate amidotransferase, in the activation of the chitin synthesis pathway in response to cell‐wall defects in Saccharomyces cerevisiae
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Medientyp:
E-Artikel
Titel:
Involvement of GFA1, which encodes glutamine–fructose‐6‐phosphate amidotransferase, in the activation of the chitin synthesis pathway in response to cell‐wall defects in Saccharomyces cerevisiae
Beteiligte:
Lagorce, Arnaud;
Le Berre‐Anton, Veronique;
Aguilar‐Uscanga, Blanca;
Martin‐Yken, Helene;
Dagkessamanskaia, Adilia;
François, Jean
Erschienen:
Wiley, 2002
Erschienen in:European Journal of Biochemistry
Sprache:
Englisch
DOI:
10.1046/j.1432-1327.2002.02814.x
ISSN:
0014-2956;
1432-1033
Entstehung:
Anmerkungen:
Beschreibung:
<jats:p>Cell‐wall damage caused by mutations of cell‐wall‐related genes triggers a compensatory mechanism which eventually results in hyperaccumulation of chitin reaching 20% of the cell‐wall dry mass. We show that activation of chitin synthesis is accompanied by a rise, from 1.3‐fold to 3.5‐fold according to the gene mutation, in the expression of most of the genes encoding enzymes of the chitin metabolic pathways. Evidence that <jats:italic>GFA1</jats:italic>, which encodes glutamine–fructose‐6‐<jats:italic>P</jats:italic>hosphate amidotransferase (Gfa1p), the first committed enzyme of this pathway, plays a major role in this process was as follows. Activation of chitin synthesis in the cell‐wall mutants correlated with activation of <jats:italic>GFA1</jats:italic> and with a proportional increase in Gfa1p activity. Overexpression of <jats:italic>GFA1</jats:italic> caused an approximately threefold increase in chitin in the transformed cells, whereas chitin content was barely affected by the joint overexpression of <jats:italic>CHS3</jats:italic> and <jats:italic>CHS7</jats:italic>. Introduction of a <jats:italic>gfa1‐97</jats:italic> allele mutation in the cell‐wall‐defective <jats:italic>gas1Δ</jats:italic> mutant or cultivation of this mutant in a hyperosmotic medium resulted in reduction in chitin synthesis that was proportional to the decrease in Gfa1p activity. Finally, the stimulation of chitin production was also accompanied by an increase in pools of fructose 6‐<jats:italic>P</jats:italic>hosphate, a substrate of Gfa1p. In quantitative terms, we estimated the flux‐coefficient control of Gfa1p to be in the range of 0.90, and found that regulation of the chitin metabolic pathway was mainly hierarchical, i.e. dominated by regulation of the amount of newly synthesized GFA1 protein. In the search for the mechanism by which <jats:italic>GFA1</jats:italic> is activated in response to cell‐wall perturbations, we could only show that neither <jats:italic>MCM1</jats:italic> nor <jats:italic>RLM1</jats:italic>, which encode two transcriptional factors of the MADS box family that are required for expression of cell‐cycle and cell‐wall‐related genes, was involved in this process.</jats:p>