Reduced expression of a distal gene of the prn gene cluster in deletion mutants of Aspergillus nidulans: Genetic evidence for a dicistronic messenger in an eukaryote

1978 ◽  
Vol 163 (1) ◽  
pp. 17-22 ◽  
Author(s):  
Herbert N. Arst ◽  
Donald W. MacDonald
1992 ◽  
Vol 12 (9) ◽  
pp. 3827-3833 ◽  
Author(s):  
T H Adams ◽  
W A Hide ◽  
L N Yager ◽  
B N Lee

In contrast to many other cases in microbial development, Aspergillus nidulans conidiophore production initiates primarily as a programmed part of the life cycle rather than as a response to nutrient deprivation. Mutations in the acoD locus result in "fluffy" colonies that appear to grow faster than the wild type and proliferate as undifferentiated masses of vegetative cells. We show that unlike wild-type strains, acoD deletion mutants are unable to make conidiophores under optimal growth conditions but can be induced to conidiate when growth is nutritionally limited. The requirement for acoD in conidiophore development occurs prior to activation of brlA, a primary regulator of development. The acoD transcript is present both in vegetative hyphae prior to developmental induction and in developing cultures. However, the effects of acoD mutations are detectable only after developmental induction. We propose that acoD activity is primarily controlled at the posttranscriptional level and that it is required to direct developmentally specific changes that bring about growth inhibition and activation of brlA expression to result in conidiophore development.


1979 ◽  
Vol 34 (1) ◽  
pp. 19-32 ◽  
Author(s):  
A. Brian Tomsett ◽  
David J. Cove

SUMMARYThe genetic fine-structure of theniiAniaD gene region ofAspergillus nidulanshas been studied using deletion mapping. Deletions were identified asniiAniaD double mutants and comprised 1% of spontaneous chlorate-resistant mutants. All such double mutants were shown to involve deletions and their frequency was not increased by mutagenic treatment with eitherN-methyl-N′-nitro-N-nitrosoguanidine or with ultraviolet light. Deletion maps of theniaD andniiA genes have been constructed. A further class of mutation was also mapped using the deletions. Thesecrnmutations, which affect a gene whose function is as yet unknown, map on the centromere proximal side ofniiA. This analysis of a eukaryote gene cluster will provide a framework upon which to base studies of the regulation of the nitrate assimilation pathway.


1987 ◽  
Vol 7 (1) ◽  
pp. 427-434
Author(s):  
B L Miller ◽  
K Y Miller ◽  
K A Roberti ◽  
W E Timberlake

Many genes that are expressed specifically in the differentiating asexual spores (conidia) of Aspergillus nidulans are organized into clusters. We investigated the effects of altered chromosomal position on expression of a gene from the conidiation-specific SpoC1 gene cluster. The gene became deregulated when integrated at nonhomologous chromosomal sites, in that transcript levels were elevated in vegetative cells (hyphae) and variably altered in conidia. We also investigated the effects on expression of insertion of the nonregulated argB gene into the SpoC1 region. Levels of argB transcripts were markedly reduced in hyphae. The results suggest that a cis-acting regional regulatory mechanism represses transcription of SpoC1 genes in hyphae. They also indicate that expression of individual SpoC1 genes is modulated during conidiation by trans-acting factors. We propose that the two types of regulation act together to produce the major differences in transcript levels observed in hyphae versus conidia.


2005 ◽  
Vol 71 (9) ◽  
pp. 5465-5475 ◽  
Author(s):  
Matthias Brock

ABSTRACT Propionate is a very abundant carbon source in soil, and many microorganisms are able to use this as the sole carbon source. Nevertheless, propionate not only serves as a carbon source for filamentous fungi but also acts as a preservative when added to glucose containing media. To solve this contradiction between carbon source and preservative effect, propionate metabolism of Aspergillus nidulans was studied and revealed the methylcitrate cycle as the responsible pathway. Methylisocitrate lyase is one of the key enzymes of that cycle. It catalyzes the cleavage of methylisocitrate into succinate and pyruvate and completes the α-oxidation of propionate. Previously, methylisocitrate lyase was shown to be highly specific for the substrate (2R,3S)-2-methylisocitrate. Here, the identification of the genomic sequence of the corresponding gene and the generation of deletion mutants is reported. Deletion mutants did not grow on propionate as sole carbon and energy source and were severely inhibited during growth on alternative carbon sources, when propionate was present. The strongest inhibitory effect was observed, when glycerol was the main carbon source, followed by glucose and acetate. In addition, asexual conidiation was strongly impaired in the presence of propionate. These effects might be caused by competitive inhibition of the NADP-dependent isocitrate dehydrogenase, because the Ki of (2R,3S)-2-methylisocitrate, the product of the methylcitrate cycle, on NADP-dependent isocitrate dehydrogenase was determined as 1.55 μM. Other isomers had no effect on enzymatic activity. Therefore, methylisocitrate was identified as a potential toxic compound for cellular metabolism.


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