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BackgroundThe genes of the non-phosphorylative L-rhamnose catabolic pathway have been identified for several yeast species. In Schefferomyces stipitis, all L-rhamnose pathway genes are organized in a cluster, which is conserved in Aspergillus niger, except for the lra-4 ortholog (lraD). The A. niger cluster also contains the gene encoding the L-rhamnose responsive transcription factor (RhaR) that has been shown to control the expression of genes involved in L-rhamnose release and catabolism.ResultIn this paper, we confirmed the function of the first three putative L-rhamnose utilisation genes from A. niger through gene deletion. We explored the identity of the inducer of the pathway regulator (RhaR) through expression analysis of the deletion mutants grown in transfer experiments to L-rhamnose and L-rhamnonate. Reduced expression of L-rhamnose-induced genes on L-rhamnose in lraA and lraB deletion strains, but not on L-rhamnonate (the product of LraB), demonstrate that the inducer of the pathway is of L-rhamnonate or a compound downstream of it. Reduced expression of these genes in the lraC deletion strain on L-rhamnonate show that it is in fact a downstream product of L-rhamnonate.ConclusionThis work showed that the inducer of RhaR is beyond L-rhamnonate dehydratase (LraC) and is likely to be the 2-keto-3-L-deoxyrhamnonate.Electronic supplementary materialThe online version of this article (doi: 10.1186/s12866-017-1118-z) contains supplementary material, which is available to authorized users.

In Aspergillus niger, the enzymes encoded by gaaA, gaaB, and gaaC catabolize d‐galacturonic acid (GA) consecutively into l‐galactonate, 2‐keto‐3‐deoxy‐l‐galactonate, pyruvate, and l‐glyceraldehyde, while GaaD converts l‐glyceraldehyde to glycerol. Deletion of gaaB or gaaC results in severely impaired growth on GA and accumulation of l‐galactonate and 2‐keto‐3‐deoxy‐l‐galactonate, respectively. Expression levels of GA‐responsive genes are specifically elevated in the ∆gaaC mutant on GA as compared to the reference strain and other GA catabolic pathway deletion mutants. This indicates that 2‐keto‐3‐deoxy‐l‐galactonate is the inducer of genes required for GA utilization.