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Appl. Environ. Microbiol. doi:10.1128/AEM.01476-06
Copyright (c) 2006, American Society for Microbiology and/or the Listed Authors/Institutions. All Rights Reserved.

The SPI1 gene, encoding a glycosylphosphatidylinositol(GPI)-anchored cell wall protein, plays a prominent role in the development of yeast resistance to lipophilic weak acids food preservatives

Biological Sciences Research Group, Centro de Engenharia Biológica e Química, Instituto Superior Técnico, 1049-001 Lisboa, Portugal

^* To whom correspondence should be addressed. Email: isacorreia{at}ist.utl.pt.

	Abstract

The Saccharomyces cerevisiae SPI1 gene encodes a member of the glycosylphosphatidylinositol (GPI)-anchored cell-wall protein family. In this work we show results indicating that SPI1 expression protects the yeast cell from damage caused by weak acids used as food preservatives. This is documented by a less extended period of adaptation to growth in their presence and by a less inhibited specific growth rate in a parental strain compared with a mutant with SPI1 deleted. Maximal protection exerted by Spi1p against equivalent concentrations of the various weak acids tested was registered for the more lipophilic acids (octanoic acid, followed by benzoic acid) being minimal for acetic acid. Weak acid-adaptation was found to involve the rapid activation of SPI1 transcription which is dependent on the presence of Msn2p transcription factor. Transcription activation of SPI1 upon acetic acid stress also requires Haa1p whereas this recently described transcription factor has a negligible role in the adaptive response to benzoic acid. The expression of SPI1 was found to play a prominent role in the development of yeast resistance to 1,3--glucanase in benzoic-acid-stressed cells while its involvement in acetic-acid induced resistance to the cell-wall lytic enzyme is slighter. Results are consistent with the notion that Spi1p expression upon weak acid stress leads to cell wall remodelling, especially for the more lipophilic acids, decreasing cell wall porosity that in turn reduces access to the plasma membrane, reducing membrane damage, intracellular acidification and viability loss.