FGSC #5857

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Mutant Type

Genus: N

reporting_genes: his-3 nic-2 al-2;cot-1;inl;pan-2

species: Neurospora crassa

allele: 1710 43002 1-112-38;C102(t);JH319;1-153-96

stock: 1710-OR20-2A

glasgow:

mutagen:

Depositor: FJD

Link Group: IR R R;IVR;VR;VIR

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-5857

ksudc_link_html: https://digital.lib.k-state.edu/item/neurospora-crassa/fgsc-5857 ↗

Genes

Locus	Cultural Requirements	Link Group	Type
cot-1	IVR. 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.	IVR	B
nic-2	IR. 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).	IR	B
pan-2	VIR. Right of rib-1 (<1 to 3%). Left of del (6%) and trp-2(11%) (140, 141, 143, 818, PB). Unable to convert ketovaline to ketopantoic acid (138, 140, 141). Used in major studies of intralocus recombination and complementation (140-143). pan-2ascospores remain white or pale if the crossing medium is not supplemented, even when the protoperithecial parent is pan-2+. Asci in which gene conversion has occurred at pan-2 can thus be recognized and isolated (1072, 1073); photographs (1072). For good recovery of pan-2progeny, crossing media should be supplemented with pantothenic acid (10 µg/ml) even when the protoperithecial parent is pan+. Called group B.	VIR	B
al-2	IR. 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).	IR	B
inl	VR. 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.	VR	B
his-3	IR. Right of met-10 (R.L. Metzenberg, personal communication). Left of cog (1 to 3%) (172,174), ure-4 (1%) (78), and ad-3A (1%) (271). (434)Requires histidine (434). Complex gene coding for histidinol dehydrogenase, phosphoribosyladenosine 5'-triphosphate-pyrophosphohydrolase, and phosphoribosyl-adenosine 5'-monophosphate-cyclohydrolase (16, 673) (Fig. 14). All three activities appear to be catalyzed by a single protein (673). Strains carrying different individual alleles may lack only the early reaction(s) or only histidinol dehydrogenase, or both. Those that lack only histidinol dehydrogenase accumulate histidinol (16, 162, 1123). Mutants produce cross-reacting material (220). Used to study intralocus complementation and recombination (15, 16, 27, 162, 164, 171, 172, 1121, 1122, 1124). Intralocus recombination is regulated by cog and by rec-2 (27, 171); it is not affected by rec-1 (172). Translocation T(IR;VII)TM429, with one breakpoint in his-3, has been used to show that cog is cis-acting (171). Initial alleles: C140 and T1710 (= C1710).	IR	B