Strain: Neurospora crassa

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FGSC #4425

Mutant Type

Genus: N

reporting_genes: cot-1;al-2;arg-12;nuc-2;inl

species: Neurospora crassa

allele: see 4411

stock:

glasgow:

mutagen:

Depositor: RLM

Link Group:

MT: a

Species No: 10

gene_back:

oppmt: 0

trans:

ref1: Metzenberg, et al NN 31:35, https://doi.org/10.4148/1941-4765.1608

ref2:

site:

country:

ksudc_link: https://digital.lib.k-state.edu/item/neurospora-crassa/fgsc-4425

ksudc_link_html: https://digital.lib.k-state.edu/item/neurospora-crassa/fgsc-4425 ↗

Genes

Locus Cultural Requirements Link Group Type
inlVR. Between pho-3 (3 to 4%) and pab-1 (1 to 10%). Right of al-3 (362, 397, 1036). (482)Requires inositol (65). Lacks D-myoinositol-1-phosphatase (1142). Lack of glucocycloaldolase found by Pina and Tatum (826) is attributed by Williams (1142) to drastic repression of glucocycloaldolase by the concentration of inositol used for growth. Growth is colonial on low levels of inositol (367). Tends to extrude dark pigment into the medium when grown on suboptimal inositol. Composition of phospholipids and cell walls is abnormal on limiting inositol (367, 439, 440, 501). Inhibited by hexachlorocyclohexane (366, 457, 931). Conidia are subject to death by unbalanced growth on minimal medium (1028, 1033), a property exploited for mutant enrichment ("inositol-less death") (606, 647) because double mutants are at a selective advantage. Heat-sensitive allele 83201 is especially useful for mutant enrichment (832, 1043). Used in the first experiments reporting transformation of Neurospora by N. crassaDNA (677, 679) and reported to be efficient as a recipient in absence of inositol (1162). Used to study glucose (917) and sulfate (641) transport systems. Used extensively for studying induced reversion (392). Used for studying the mechanism of inositol-less death (647, 702), mutagenicity of ferrous ions, and regulation of mitochondrial membrane fluidity; for a review, see reference 702. Spontaneous reversion rates (386). Allele-specific partial suppressor (390). Allele 46802 is nonrevertable and inseparable from translocation 46802 (386, 808). Strains carrying heat-sensitive allele 83201 show slow semicolonial growth in liquid minimal medium at 25°C (641), but look normal on slants (D.D. Perkins, unpublished data). Strains carrying allele 89601 contain cross-reacting material (1183). Mutant gene exo-1 is present in the inl(89601) a stock FGSC 498 and may, therefore, be present in stocks of mutants derived by inositol-less death. (See references 194, 325, and 1027). Called inos.VRB
nuc-2IIR. Between the T(NM177) breakpoints; hence, right of aro-3. Left of preg(1 to 2%) and pe (4%). Probably allelic with pcon (0/854) (593, 671). (514) Unable to use RNA or DNA as a phosphorus source (514). Defective in production of repressible alkaline and acid phosphatases (671, 1077). Several nucleases absent or reduced (449). Interaction with other phosphate regulatory genes (665). Recessive to nuc+ in partial diploids and heterokaryons (671). Not defective in nuh function (538). Scored on low-phosphate medium by a staining reaction with alpha-naphthyl phosphate plus diazo blue B (397, 1077), by failure to grow on minimal medium altered so that 0.1 g of RNA or DNA per liter is substituted for the inorganic phosphate source (514, 538), or by failure to grow on low-phosphate medium at a pH above 7 (R.L. Metzenberg, personal communication). Used to study phosphate transport (624). For a regulation model, see references 665 and 670. See pcon.IIRB
arg-12Uses arginine or citrulline.IIRB
al-2IR. Right of os-5 (<1%) and T(STL76). Left of arg-6(1%) and al-1 (797, 802, 808, 816, 818). Included in duplications from Tp(T54M94), confirming location left of arg-6(808). (482) Carotenoids absent or abnormal, but steroids produced (398). Blocked in microsomal fraction and defective in phytoene synthetase (445), a particulate enzyme (445 and references cited therein) (Fig. 9). Tracer experiments indicate a lesion between prephytoene pyrophosphate and phytoene (572). Alleles include those resulting in white and pale rose-white, e.g., 15300 and Y254MI65 (1042), and purple, e.g., MN58a (154). For complementation, see references 500 and 1041. Fine-structure mapping (500, 1042) needs reevaluation because of new information on the location of the arg-6 marker (797).IRB
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

Neurospora Crassa Wikipedia

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