A co-activator of nitrogen-regulated transcription in Saccharomyces cerevisiae.

In Saccharomyces cerevisiae, the transcription factors Gln3p and Nil1p of the GATA family play a determinant role in expression of genes that are subject to nitrogen catabolite repression. Here we report the isolation of a new yeast mutant, gan1-1, exhibiting dramatically decreased NAD-linked glutamate dehydrogenase (NAD-GDH) and glutamine synthetase (GS) activities. The GAN1 gene was cloned and found to encode a 488-amino-acid polypeptide bearing no typical DNA binding domain. Gan1p is required for full expression of GLN1, GDH2 and also other nitrogen utilization genes, including GAP1, PUT4, MEP2 and GDH1. The extent to which Gan1p is required, however, varies according to the gene and to the nitrogen source available. We show that Gan1p is in fact involved in Gln3p- and Nil1p-dependent transcription. In the case of Gln3p-dependent transcription, the degree to which Gan1p is required appears to be gene specific. The contribution of Gan1p to gene expression is also influenced by the nitrogen status of the cell. We found that GAN1 is identical to ADA1, which encodes a component of the ADA/GCN5 co-activator complex. Ada1/Gan1p thus represents the first reported case of an accessory protein (a co-activator) linking the GATA-binding proteins Gln3p and Nil1p, mediating nitrogen-regulated transcription, to the basal transcription machinery.Journal ArticleResearch Support, Non-U.S. Gov'tFLWINinfo:eu-repo/semantics/publishe

Styrene, an Unpalatable Substrate with Complex Regulatory Networks

Styrene, a volatile organic compound (VOC), is an important industrial material involved in the production of plastic, synthetic rubber and resin, insulation and other industrial materials containing molecules such as polystyrene, butadiene-styrene latex, styrene copolymers and unsaturated polyester resins. Styrene exposure may cause contact-based skin inflammation, irritation of eyes, nose and respiratory tract. Neurological effects such as alterations in vision, hearing loss and longer reaction times, have been associated with styrene exposure in the workplace. In addition, styrene oxide may act as an established mutagen and carcinogen (www.epa.gov/chemfact/styre-sd.pdf). It has been reported that, in 2002, 22,323 tons of styrene were released to the environment (82), in spite of the US Clean Air Act mandate on reduction in the volume of allowable styrene emission (www.epa.gov/chemfact/styre-sd.pdf). Among a variety of emerging air pollution technologies, biofiltration is an attractive option for the treatment of VOCs, because it is cost-effective and does not generate secondary contaminants (45). Moreover, microbial biodegradation is the major route for the removal of non-aqueous compounds from soils. Styrene is also naturally present in non polluted environments, since it derives from fungal decarboxylation of cinnamic acid (90). Therefore it is not surprising that microorganisms of different families have been found to be able to degrade this compound (31). The promising results obtained in the removal of styrene from contaminated waste-gases by biofiltration (5, 39, 103) have led to an increasing attention to the regulatory mechanisms underlying styrene degradation, with the aim to improve bioremediation processes. Despite the diffusion in nature of this degradative capability, only few strains, mainly belonging to the Pseudomonas genus, have been characterized (66). This chapter is focused on the up-to-now discovered regulatory mechanisms underlying the expression of the styrene-catabolism genes. Moreover, open questions on environmental and metabolic constrains that govern styrene degradation are discussed. Biotechnological relevance of styrene-degrading strains in fine chemicals production and bioremediation processes is not examined here. Main topics on these application fields have recently been reviewed by Dobson and co-workers (66)