A phosphoglucose isomerase mutant in Aspergillus nidulans is defective in hyphal polarity and conidiation.

Upon germination Aspergillus nidulans swoM1 exhibits abnormal development by extending a primary germ tube that quickly reverts to isotropic growth and results in an enlarged, swollen apex with pronounced wall thickenings. Apical lysis occurs in 38% of the germlings. A point mutation in the AN6037.3 gene encoding the only phosphoglucose isomerase in A. nidulans is responsible for the defect. Loss of polarity is bypassed when glucose is replaced with alternate carbon sources but in all cases the mutant is unable to conidiate due to a block in conidiophore development at vesicle formation. In conidiophores SwoM::GFP localizes to multiple punctate, foci within each actively growing cell type, and to multiple foci in mature dormant conidia. In hyphae SwoM::GFP localized to two rings spanning the center of mature septa. In hyphae localization is concentrated at actively growing hyphal tips.