The Neurospora circadian clock-controlled gene, ccg-2, is allelic to eas and encodes a fungal hydrophobin required for formation of the conidial rodlet layer.

Dec 1, 1992Genes & development

The fungal gene controlling daily rhythms, ccg-2 (also called eas), makes a protein needed to form the protective outer layer of spores

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Abstract

The ccg-2 gene is transcriptionally activated in a time-of-day-specific manner by the circadian clock.

The predicted Ccg-2 polypeptide shows significant similarity to hydrophobins, proteins involved in spore surface structure.
Allelic relationships between ccg-2 and the easily wettable (eas) locus are supported by genetic linkage and functional complementation.
Transformation of an eas mutant strain with ccg-2 DNA restores the production of surface rodlets.
Inactivation of the ccg-2 gene leads to an eas phenotype, characterized by the loss of rodlet fascicles.
The eas mutant exhibits dramatically reduced levels of ccg-2 mRNA without affecting the circadian clock's normal function.
The expression of ccg-2 is light-induced, highlighting the interplay between light and the circadian clock in fungal spore development.

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The Neurospora crassa clock-controlled gene (ccg-2) is transcriptionally activated by the circadian clock in a time-of-day-specific manner. Transcript and sequence analyses of ccg-2 reveal that the predicted Ccg-2 polypeptide bears significant similarity to a class of low-molecular-weight, cysteine-rich, hydrophobic proteins (hydrophobins), first identified in Schizophyllum, and including the product of the developmentally regulated Aspergillus gene, rodletless, required for spore surface rodlets. Allelism between ccg-2 and easily wettable (eas) (one of the first developmental genetic loci identified in Neurospora) was predicted on the basis of this similarity, their close genetic linkage, and previous findings demonstrating that eas mutants lack rodlets. In this study allelism is confirmed experimentally by showing that (1) transformation of an eas mutant strain with ccg-2 DNA results in phenotypic complementation, including restoration of surface rodlets, (2) inactivation of the ccg-2 gene, by RIP, results in an eas phenotype including loss of rodlet fascicles, and (3) the original eas strain has dramatically reduced levels of ccg-2 mRNA. Thus, the clock-controlled ccg-2 gene encodes an integral component of fungal asexual spores important for spore dispersal. The dramatic reduction of ccg-2 expression in the eas mutant has no apparent effect on the normal operation of the circadian clock, confirming that there is no feedback of this clock output on the oscillator itself. These data, in conjunction with the previous observation that ccg-2 is light induced, serve to focus attention on the dual interacting role of light and the circadian clock in the regulation of fungal spore development.

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The Neurospora circadian clock-controlled gene, ccg-2, is allelic to eas and encodes a fungal hydrophobin required for formation of the conidial rodlet layer.

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