Disease relevance of Neurospora

• The neurospora CYT-18 protein suppresses defects in the phage T4 td intron by stabilizing the catalytically active structure of the intron core [1].
• Therefore, these fungal enzymes have been termed "bifunctional." We have cloned chorismate synthase from the common bread mold Neurospora crassa, expressed it heterologously in Escherichia coli, and purified it in a three-step purification procedure to homogeneity [2].
• The genes al-1 and crtI mediate the desaturation of phytoene in Neurospora crassa and Rhodobacter capsulatus, respectively [3].
• Rapid RNA sequencing: nucleases from Staphylococcus aureus and Neurospora crassa discriminate between uridine and cytidine [4].
• The Neurospora crassa metallothionein (NC) synthesis gene was cloned and expressed in Escherichia coli in two different expression vectors (pING2 and pUA7), both under the regulation of the Salmonella typhimurium arabinose operon [5].

High impact information on Neurospora

• vvd, a gene regulating light responses in Neurospora, encodes a novel member of the PAS/LOV protein superfamily [6].
• One of these, SDE1, is a plant homolog of QDE-1 in Neurospora crassa that encodes an RNA-dependent RNA polymerase [7].
• Thus, in both the phasing of dark expression and the response to light mPer1 is most similar to the Neurospora clock gene frq [8].
• By fusing the encoding presequence of subunit 9 of the Neurospora ATPase to a restriction fragment containing the bI4 maturase coding sequence, we have constructed a hybrid gene that can be translated on yeast cytosolic ribosomes [9].
• The group I intron in the Neurospora mitochondrial large rRNA gene is not self-splicing in vitro [10].

Chemical compound and disease context of Neurospora

• Carotenoid desaturases from Rhodobacter capsulatus and Neurospora crassa are structurally and functionally conserved and contain domains homologous to flavoprotein disulfide oxidoreductases [3].
• E. coli shikimate dehydrogenase is homologous to the shikimate dehydrogenase domain of the fungal arom multifunctional enzymes and to the catabolic quinate dehydrogenase of Neurospora crassa [11].
• Hyperthermia, CdCl2, sodium arsenite, and H2O2 led to the rapid appearance of high levels of peroxidase in Neurospora crassa cultures and induced tolerance toward normally lethal temperatures in 60-h-old colonies [12].
• FDH was tested for the presence of nitrogenase-type cofactor and nitrate reductase-type cofactor by the Azotobacter vinelandii UW-45 and Neurospora crassa nit-1 reconstitution assays, respectively [13].
• Some of the ammonium released is assimilated back into glutamine, indicating that a glutamine cycle similar to that in Neurospora operates in Rhizobium [14].

Biological context of Neurospora

• RNA splicing in neurospora mitochondria: self-splicing of a mitochondrial intron in vitro [15].
• We have demonstrated previously that dim-2 encodes a DNA methyltransferase that is responsible for all known cytosine methylation in Neurospora crassa [16].
• The Neurospora CYT-18 protein, the mitochondrial tyrosyl-transfer RNA synthetase (mt TyrRS), promotes splicing of the Neurospora mitochondrial large ribosomal RNA (LSU) and other group I introns by stabilizing the catalytically active structure of the intron core [17].
• Recent studies indicate that DNA methylation in Neurospora depends on one DNA methyltransferase, DIM-2 (ref. 6), directed by a histone H3 methyltransferase, DIM-5 (ref. 7), but little is known about its cellular and evolutionary functions [18].
• Posttranscriptional gene silencing in Neurospora by a RecQ DNA helicase [19].

Anatomical context of Neurospora

• Structure and function of initiator methionine tRNA from the mitochondria of Neurospora crassa [20].
• Chloramphenicol-sensitive labelling of protein in microsomes of Neurospora crassa [21].
• Chitin synthase 1 plays a major role in cell wall biogenesis in Neurospora crassa [22].
• The Neurospora vacuolar ATPase showed no crossreactivity with antiserum to plasma membrane or mitochondrial ATPase but strongly crossreacted with antiserum against a polypeptide of Mr approximately equal to 70,000 associated with the tonoplast ATPase of corn coleoptiles [23].
• The H+-translocating ATPase located on vacuolar membranes of Neurospora crassa was partially purified by solubilization in two detergents, Triton X-100 and N-hexadecyl-N,N-dimethyl-3-ammonio-1-propanesulfonate, followed by centrifugation on sucrose density gradients [23].

Associations of Neurospora with chemical compounds

• In mammals, methylation is almost exclusively in the under-represented CpG dinucleotides, and most CpGs are methylated whereas in Neurospora, methylation is not preferentially in CpG dinucleotides and the bulk of the genome is unmethylated [18].
• Circadian periodicity a neurospora: alteration by inhibitors of cyclic AMP phosphodiesterase [24].
• Three methyl xanthine inhibitors of adenosine 3',5'-monophosphate phosphodiesterase-theophylline, aminophyline, and caffeine-lengthen the period of the circadian conidiation rhythm of Neurospora [24].
• Novel mechanisms controlling arginine metabolism in Neurospora [25].
• METHODS: We tested the ability of zebularine to reactivate a silenced Neurospora crassa gene using a hygromycin gene reactivation assay [26].

Gene context of Neurospora

• We cloned, sequenced and physically mapped the MAS20 gene and found that the protein is homologous to the MOM19 import receptor from Neurospora crassa [27].
• We isolated the TIM23 complex of Neurospora crassa [28].
• Although some continuity in the chromosomal location of the MAT locus can be traced throughout hemiascomycete evolution and even to Neurospora, the gene content of the locus has changed with the loss of an HMG domain gene (MATa2) from the MATa idiomorph shortly after HO was recruited [29].
• The remaining three residues, Trp-120, Leu-123, and Phe-124, are highly conserved between GCN4 and its Neurospora counterpart, cpc-1 [30].
• Of particular interest is the comparable increase in a nuclease under the control of the RAD52 gene; this enzyme has been identified by the use of antibody raised against a similar enzyme from Neurospora crassa [31].

Analytical, diagnostic and therapeutic context of Neurospora

• Molecular cloning and characterization of cytochrome c cDNA clones of Neurospora crassa wild-type (74A) and a cytochrome c-deficient mutant (cyc1-1) are described [32].
• Site-directed mutagenesis of the cysteine residues in the Neurospora crassa plasma membrane H(+)-ATPase [33].
• Liposomes prepared by sonication of asolectin were fractionated by glycerol density gradient centrifugation, and the small liposomes contained in the upper region of the gradients were used for reconstitution of purified, radiolabeled Neurospora plasma membrane H+-ATPase molecules by our previously published procedures [34].
• After autoradiography, the base-paired nucleotides are definitively located by comparing V1 generated bands with fragments of known length produced by both Neurospora endonuclease and base-specific ribonucleases [35].
• Three-dimensional structure of NADH: ubiquinone reductase (complex I) from Neurospora mitochondria determined by electron microscopy of membrane crystals [36].

References