Characteristics of physiological inducers of the ethanol utilization (alc) pathway in Aspergillus nidulans

Abstract

The ethanol utilization (alc) pathway in Aspergillus nidulans is one of the strongest expressed gene systems in filamentous fungi. The pathway-specific activator AlcR requires the presence of an inducing compound to activate transcription of genes under its control. We have demonstrated recently that acetaldehyde is the sole physiological inducer of ethanol catabolism. In the present study we show that compounds with catabolism related to that of ethanol, i.e. primary alcohols, primary monoamines and l-threonine, act as inducers because their breakdown results in the production of inducing aliphatic aldehydes. Such aldehydes were shown to induce the alc genes efficiently at low external concentrations. When ethanol is mixed with representatives of another class of strong direct inducers, ketones, the physiological inducer, acetaldehyde, prevails as effector. Although direct inducers essentially carry a carbonyl function, not all aldehydes and ketones act as inducers. Structural features discriminating non-inducing from inducing compounds concern: (i) the length of the aliphatic side group(s); (ii) the presence and nature of any non-aliphatic substituent. These characteristics enable us to predict whether or not a given carbonyl compound will induce the alc genes.

Ethanolamine Catabolism in Pseudomonas aeruginosa PAO1 Is Regulated by the Enhancer-Binding Protein EatR (PA4021) and the Alternative Sigma Factor RpoN

“…In this microorganism, AlcR is a regulator of ethanol catabolism that responds directly to acetaldehyde and upregulates the transcription of genes encoding alcohol (alcA) and aldehyde (aldA) dehydrogenases (53,54). Similar to the situation described herein for P. aeruginosa PAO1, growth on compounds that are degraded into acetaldehyde induce expression of the alcA and aldA genes in Aspergillus nidulans (55,56). Additionally, the aldehyde intermediates generated from the catabolism of other compounds, such as D-galacturonic acid and putrescine, also induce expression of the alcA and aldA genes (56).…”

Inducer-Dependent Nuclear Localization of a Zn(II)2Cys6Transcriptional Activator, AmyR, inAspergillus nidulans

“…The fusion gene was placed under the control of the A. nidulans alcA promoter, which enables expression of the fusion gene at desired time points by the addition of inducers for alcA expression, such as ethylmethylketone (EMK) and threonine. 39) The fusion gene was targeted in single copy to the argB locus of the A. nidulans malA1 mutant MA1. The genetically identified malA gene encodes AmyR, and the malA1 allele carries a loss of function mutation (H478 to L) in AmyR.…”

Genetic Interactions of the Aspergillus nidulans atmAATM Homolog With Different Components of the DNA Damage Response Pathway

“…As first step, we validate the alcATatmA construction in the wild-type strain ( Figure 1). The alcA promoter is induced to high levels by glycerol, ethanol, and l-threonine and repressed by glucose (Flipphi et al 2002). The construction (p)alcAT gfpTatmA 1kb was transformed into the wild-type strain and several transformants were obtained in which the plasmid had integrated homologously (as verified by PCR) and produced a functional GfpTAtmA when derepressed with glycerol ( Figure 1A).…”