Successful beyond expectation: David Perkins's research with chromosome rearrangements in Neurospora

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B2B-2K5: the new buzz in translational research

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Magic with moulds: meiotic and mitotic crossing over in Neurospora inversions and duplications

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Het up mould unleashes a sporekiller prion

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Benign anomaly to malign dysplasia: variable expression of lamin B receptor mutations in humans

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Blueprint of a red mould: unusual and unexpected findings in the Neurospora genome sequence

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Nondegradative pisatin resistance in Dictyostelium discoideum, Neurospora crassa and Nectria haematococca: similarities and differences

Paradoxically, on pisatin-medium (150 µg/ml) the cellular slime mouldDictyostelium discoideum grows only when plated as spores but not when plated as amoebae. The recent discovery of inducible nondegradativc pisatin resistance in amoebae has allowed us to formulate a model that resolves this paradox. In this model, the germinating amoeba is postulated to acquire a pisatin-resistance phenotype while ensconced within the spore wall. This article reviews the findings on which this model is based and extends it to also account for the differences in pisatin sensitivity phenotype that result from sterol alteration in cellular slime moulds and fungi

Genes encoding chimeras of Neurospora crassa erg-3 and human TM7SF2 proteins fail to complement Neurospora and yeast sterol C-14 reductase mutants

The human gene TM7SF2 encodes a polypeptide (SR-1) with high sequence similarity to sterol C-14 reductase, a key sterol biosynthetic enzyme in fungi, plants and mammals. In Neurospora and yeast this enzyme is encoded by the erg-3 and erg24 genes respectively. In an effort to demonstrate sterol C-14 reductase activity for SR-1 we constructed six recombinant genes coding for chimeras of the Neurospora erg-3 and SR-1 protein sequences and tested them for complementation of the Neurospora erg-3 mutant. To our surprise, all the chimeras failed to complement erg-3. A few of the chimeric proteins were also tested against the yeast erg24 mutant, but again there was no complementation. We discuss some reasons that might account for these unexpected findings

Collateral damage: spread of repeat-induced point mutation from a duplicated DNA sequence into an adjoining single-copy gene in Neurospora crassa

Repeat-induced point mutation (RIP) is an unusual genome defense mechanism that was discovered in Neurospora crassa. RIP occurs during a sexual cross and induces numerous G:C to A:T mutations in duplicated DNA sequences and also methylates many of the remaining cytosine residues. We measured the susceptibility of theerg-3 gene, present in single copy, to the spread of RIP from duplications of adjoining sequences. Genomic segments of defined length (1, 1.5 or 2 kb) and located at defined distances (0, 0.5, 1 or 2 kb) upstream or downstream of theerg-3 open reading frame (ORF) were amplified by polymerase chain reaction (PCR), and the duplications were created by transformation of the amplified DNA. Crosses were made with the duplication strains and the frequency of erg-3 mutant progeny provided a measure of the spread of RIP from the duplicated segments into the erg-3 gene. Our results suggest that ordinarily RIP-spread does not occur. However, occasionally the mechanism that confines RIP to the duplicated segment seems to fail (frequency 0.1-0.8%) and then RIP can spread across as much as 1 kb of unduplicated DNA. Additionally, the bacterialhph gene appeared to be very susceptible to the spread of RIP-associated cytosine methylation

Why are Neurospora crassa crosses that are homozygous for a large duplication barren?

Crosses homozygous for the duplication Dp(AR17) are barren regardless of RIP. Sad-1, a semi-dominant suppressor of meiotic silencing, suppresses the barrenness of duplication-heterozygous but not of duplication-homozygous crosses. Could it be that in the context of the homozygous cross the sad-1+ allele is not detected as being unpaired, and consequently, Sad-1 fails to suppress meiotic silencing