Aspergillus nidulans mutant lacking alpha-(1,3)-glucan, melanin, and cleistothecia

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Abstract
A mutation in A. nidulans led to a loss of both melanin and .alpha.-(1,3)-glucan, a major wall polysaccharide. The mutation prevented the formation of cleistothecia. Mutant walls contained increased amounts of .beta.-(1,3)-glucan and galactose polymers, and electron micrographs indicated that they had lost the outermost wall layer. Such walls were more readily digested by lytic enzymes, and this increased susceptibility to hydrolysis was due to the absence of .alpha.-(1,3)-glucan and not of melanin. The pleiotropic effects of the mutation are discussed, with particular reference to the hypothesis that .alpha.-(1,3)-glucan acts as the endogenous C source for biosynthetic processes in the stationary phase of growth. In this view, glucan synthesis would be the primary target of the mutation, and the absence of glucan would result in the lack of melanin and cleistothecia, formed after nutrients are exhausted. Two other mutations that lowered the mycelial .alpha.-(1,3)-glucan content also inhibited melanin and cleistothecia production.