Strain: Neurospora crassa

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FGSC #256

Mutant Type

Genus: N

reporting_genes: ad-5 nic-2 thi-1;cot-1

species: Neurospora crassa

allele: Y152M40 43002;56501;C102(t)

stock: 1287

glasgow:

mutagen:

Depositor: DDP

Link Group: IL IR IR;IVR

MT: A

Species No: 10

gene_back:

oppmt: 0

trans:

ref1:

ref2:

site:

country:

ksudc_link: https://digital.lib.k-state.edu/item/neurospora-crassa/fgsc-256

ksudc_link_html: https://digital.lib.k-state.edu/item/neurospora-crassa/fgsc-256 ↗

Genes

Locus Cultural Requirements Link Group Type
cot-1IVR. Between pan-1 (2%) and his-4 (1 to 6%) (692, 812, 816). Extremely colonial at 34°C, but completely normal growth, morphology, and fertility at 25°C and below. Linear growth is maximum at 24°C (374). Becomes colonial at 32°C; colonies from ascospores or conidia are viable and continue to grow slowly with dense branching, but do not conidiate. They quickly resume normal growth when shifted to a permissive temperature (692, 1068). Recessive in duplications (808); apparent dominance in heterokaryons (374) may have resulted from a shift in nuclear ratios. Used in studies of septation and branching (202), growth-inhibiting mucopolysaccharide (878, 879), and sulfate transport (641). Cell wall analysis (374). Growth is stimulated by lysine or arginine (0.1 mM) on glucose media at high temperatures (615). Because of high viability and tightly restricted growth at restrictive temperatures and normality at 25°C, cot-1 mutants have valuable technical applications. For example, crosses homozygous for cot-1 have been used in combination with sorbose for experiments with rec genes, where high-density ascospore platings are required for precise quantitative analysis of intralocus recombination (e.g., references 165, 997, and 1070). In another application, when shifted up after initial growth at the permissive low temperature, cot-1hyphae assume a "bottle brush" appearance with small side branches (692). This has been used to select uvs mutants by subsurface survival on UV-irradiated plates containing p-aminobenzoic acid (938; D.E.A. Catcheside, personal communication). cot-1 conidia or ascospores from cot-1 x cot-1crosses are used for replication in a protocol involving transfer by filter paper (615). For suppressors of cot-1, see gul.IVRB
nic-2IR. Between ad-3B (4%) and ace-7 (4 to 7%) (271, 578). (482) Grows on nicotinic acid, nicotinamide, or high concentrations of quinolinic acid (97, 1168). Cannot use kynurenine, hydroxykynurenine, or hydroxyanthranilic acid (96, 1168). Accumulates 3-hydroxyanthranilic acid (96) (Fig. 18). Aging cultures accumulate red-brown pigment in the medium. Used to study intralocus recombination (908). Translocations T(4540) and T(S1325)are inseparable from nic-2 (808, 908, 911).IRB
thi-1IR. Right of the T(4540) right breakpoint and cys-9 (13%). Left of T(NM103), T(ALS182), and met-6 (7 to 14%) (721, 808, 816, 1091). (482). Uses thiamine or precursors pyrimidine plus thiazole (1059). Adaptation to growth on minimal medium occurs after a lag; growth tests should, therefore, be scored early. Adaptation is not carried over via ascospores, conidia, or small mycelial fragments. Adaptive growth is paralleled by attainment of wild-type thiamine pyrophosphate and carboxylase levels. Apparently concerns utilization of intact thiamine rather than its biosynthesis. (302, 303). Allele 17084 is inseparable from translocation T(IR;VII)17084 (808).IRB
ad-5IL. Between phe-1 and arg-1 (1%) (816; H.B. Howe, Jr., personal communication). (482) Uses adenine or hypoxanthine (682) (Fig. 8). Accumulates AICAR (81, 904) and SAICAR (81). Some mutants are stimulated by histidine and may not grow on hypoxanthine unless histidine is present; others may be inhibited by histidine (393; M.E. Case, personal communication). Produces some purple pigment, but less than ad-3A and ad-3Bmutants (526). Called complementation group J. Evidence, apparently enzymatic, given in reference 120 suggests that some ad-5 mutants lack both AICAR formyltransferase and inosine 5'-monophosphate cyclohydrolase, but apparently other ad-5 mutants lack only the formyltransferase. Indirect evidence (902, 904) suggests that strains carrying ad-5 allele Y112M192 are blocked at the formyltransferase step.ILB

Neurospora Crassa Wikipedia

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