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In <i>Aspergillus nidulans</i> L-rhamnose is catabolised to pyruvate and L-lactaldehyde, and the latter ultimately to L-lactate, via the non-phosphorylated pathway (LRA) encoded by the genes <i>lraA</i>-<i>D</i>, and <i>aldA</i> that encodes a broad substrate range aldehyde dehydrogenase (ALDH) that also functions in ethanol utilisation. LRA pathway expression requires both the pathway-specific transcriptional activator RhaR (<i>rhaR</i> is expressed constitutively) and the presence of L-rhamnose. The deletion of <i>lraA</i> severely impairs growth when L-rhamnose is the sole source of carbon and in addition it abolishes the induction of genes that respond to L-rhamnose/RhaR, indicating that an intermediate of the LRA pathway is the physiological inducer likely required to activate RhaR. The loss-of-function mutation <i>aldA67</i> also has a severe negative impact on growth on L-rhamnose but, in contrast to the deletion of <i>lraA</i>, the expression levels of L-rhamnose/RhaR-responsive genes under inducing conditions are substantially up-regulated and the production of α-L-rhamnosidase activity is greatly increased compared to the <i>aldA</i>⁺ control. These findings are consistent with accumulation of the physiological inducer as a consequence of the loss of ALDH activity. Our observations suggest that <i>aldA</i> loss-of-function mutants could be biotechnologically relevant candidates for the over-production of α-L-rhamnosidase activity or the expression of heterologous genes driven by RhaR-responsive promoters.