Free-living cells monitor extracellular 'osmotic strength' and respond metabolically to offset unfavourable osmotic intracellular solute concentrations. Here, we report the reconstruction of the Aspergillus nidulans salt stress-controlling MAP kinase pathway, based on homology analysis with known yeast genes. In A. nidulans, salt stress HOG genes, such as pbsA, hogA, ptpA and msnA, are upregulated when exposed to high concentrations of salt and, in a hogA deletion mutant (SIK1), the accumulation of pbsA is strongly reduced, suggesting a salt-specific feedback induction mechanism. Growth of SIK1 appears to be unchanged in unstressed cells, but hyphal extension rates are reduced by as much as 60% in the presence of salt. Microscopic observation revealed abnormal hyperbranched hyphal tips, disproportionate accumulation of nuclei and absence of septa. Thus, the inability to maintain turgor pressure depresses cell expansion and results in slower volume increases. In addition, SIK1 fails to partition the apical cell; thus, nuclei are not likely to arrest mitosis in interphase as in normal cells, but continue to divide, accumulating to high levels.