FGSC #7868

Mutant Type

Genus: N

reporting_genes: (fr nit-2 A + a[m1] ad-3B cyh-1)

species: Neurospora crassa

allele: B110 nr7

stock: 1747

glasgow:

mutagen:

Depositor: DDP

Link Group: IL IL

MT: A

Species No: 10

gene_back: SL

oppmt: 0

trans:

ref1:

ref2:

site:

country:

ksudc_link: https://digital.lib.k-state.edu/item/neurospora-crassa/fgsc-7868

ksudc_link_html: https://digital.lib.k-state.edu/item/neurospora-crassa/fgsc-7868 ↗

Genes

Locus	Cultural Requirements	Link Group	Type
ad-3B	IR. Between ad-3A (0.1 to 0.7%) and nic-2 (3%) (271). (482) Uses adenine or hypoxanthine (682). Blocked in interconversion of AIR to CAIR (348) (Fig. 8). Produces purple pigment, permitting direct visual selection (276, 682). Pigment is secreted with low concentrations of adenine (e.g., 0.1 mM), not with high concentrations (2 mM) (276, 682, 785). Pigment production used to assess effect of histidine and tryptophan on purine nucleotide synthesis (786). Reduced interallelic fertility (264, 407). Complementation maps (268, 274). Relation of mutagens to complementation patterns (269). Mutants with non-polarized complementation patterns on the right side of the complementation map grow on minimal medium if supplied with CO2; other mutants do not respond to CO2, (270). Used extensively for mutagenesis (see ad-3A). Rearrangement T(I- >III)Y112M4i ad-3B, which has a breakpoint inseparable from ad-3B, was the first insertional translocation to be reported for fungi (266). Allele 7-017-0137 shows "fixed instability," mutating to an unstable prototrophic allele (41). Alleles 2-17-126, 12-21-28, and numerous others are supersuppressible (408, 749, 955). Called complementation group B.	IR	B
am1			B
cyh-1	IR. Right of nit-1 (6%). Left of T(STL76) and al-2 (8 to 13%) (496, 797, 808).Resistant to cycloheximide (496, 748). Resistance is recessive in duplications (1090). Dominance reported in forced heterokaryons (496, 748) may have been due to skewed nuclear ratios (1090). Protein synthesis on ribosomes of the mutant cyh-1 proceeds in the presence of cycloheximide in a cell-free system (834). Readily scored on slants with 10 µg of cycloheximide per ml autoclaved in the medium. Excellent as a marker and valuable for selecting somatic recombinants or deletions in heterozygous duplications (748, 1091). Used to show that the cycloheximide-induced phase shift of the circadian clock involves protein synthesis (738). Called act-1: actidione resistant-1.	IR	B
fr	IL. Between ro-10 (18%) and un-5 (6%) (798, PB). (789)Delicate branching on agar surface and delicate aerial growth with no conidia (789). Multiple hyphal branching (382). Deficient in glucose- 6-phosphate dehydrogenase (as are col-2 and balmutants) (949, 952). Partially deficient in linolenic acid (115); morphology partially corrected by exogenous linolenic acid (892, 943). Low adenylate cyclase activity and low adenosine 3',5'-phosphate (943, 950). Used to determine what functions are controlled by adenosine 3',5'-phosphate (779). Unlike cr-1, fr is not corrected morphologically by exogenous cyclic nucleotides (892, 951). Scott (943) reported that morphology is corrected by theophylline; Rosenberg and Pall (892) reported no correction by phosphodiesterase inhibitors. Cell wall analysis; photograph (112, 278, 946). Reduced amount of cell wall peptides (1165). Recessive in duplications (808). Female sterile. Both known alleles (B110 and R2499) revert to fr+.	IL	B
nit-2	IL. Right of the T(39311) left breakpoint and of un-5(2%). Left of In(OY323) and leu-3 (12 to 18%) (57, 808, 816, PB). (335, 1135) Cannot use nitrate, nitrite, purines, or most amino acids as a nitrogen source but will grow on ammonia, glutamine, or glutamate. nit-2+ is a major nitrogen control gene and mediates nitrogen catabolite repression. The nit-2 mutant is missing (or has severely reduced levels of) nitrate reductase, nitrite reductase, uricase, xanthine dehydrogenase, allantoinase, allantoicase, L-amino acid oxidase, general amino acid permease, extracellular protease, and an intracellular neutral phenylmethylsulfonyl fluoride-sensitive protease (227, 324, 441, 872, 1001, and references therein). Also affects levels of glutamate dehydrogenases (226) and uptake of uracil and uridine (128). Prevents leaky growth of the mutant am on minimal medium (155). The product of the nit-2gene has been tentatively identified as a nuclear DNA-binding protein, whose affinity for DNA is reduced in the presence of glutamine (433). Allele K31 (called pink) originated in N. sitophila and was introgressed into N. crassa (335); protein product of K31 may show altered mobility (433). Recombination within the nit-2 locus is subject to regulation by rec-1 (157). Heterozygosity for closely linked ss reduces recombination within nit-2 (161). Called amr: ammonium regulation in reference 872.	IL	B
A			B