FGSC #281

Mutant Type

Genus: N

reporting_genes: al-2;fl;sc;pan-1;inl;ylo-1;nt

species: Neurospora crassa

allele: 15300;L;5801;5531;37401;Y30539y;C86

stock: 9021

glasgow:

mutagen:

Depositor: DDP

Link Group: IR;IIR;IIIR;IVR;VR;VIL;VIIR

MT: a

Species No: 10

gene_back:

oppmt: 0

trans:

ref1: Perkins 1959 Genetics 44:1185-1208, https://www.genetics.org/content/44/6/1185.long

ref2:

site:

country:

ksudc_link: https://digital.lib.k-state.edu/item/neurospora-crassa/fgsc-281

ksudc_link_html: https://digital.lib.k-state.edu/item/neurospora-crassa/fgsc-281 ↗

Genes

Locus	Cultural Requirements	Link Group	Type
fl	IIR. Between ace-1 (5 to 11%) and trp-3 (3%) (816, PB). (613)No macroconidia (609). Highly fertile (612). Used routinely as the female parent in tests for chromosome rearrangements and for mating type (e.g., reference 801). The flsingle mutant produces few microconidia when dry; when wetted, sufficient microconidia are produced to have been used in early irradiation and mutation studies (614, 915); large numbers can be obtained under certain conditions; see reference 893. pe fl (46, 700) and fl;dn (806) double mutants produce abundant microconidia; the latter combination is highly fertile when homozygous. Photograph of microconidial formation (774); see also reference 893. Nuclear numbers in microconidia (46, 64, 478). Wall analysis (207). Immunoelectrophoretic pattern (784). Paradoxical high alcoholic glycolysis on nitrate medium (80). Deficiency of isocitrate lyase on acetate medium; see citations in reference 1088. When fl A and fl a strains are inoculated separately on crossing medium in plates, a double line of perithecia forms where they meet, similar to that accompanying barrage in Podospora (410, 414). fl ascospores from certain fl x fl+ crosses often germinate spontaneously (1127; N. B. Raju, personal communication). Allele C-1835 was called acon (717, 812).	IIR	B
ylo-1	VIL. Between cys-1 (8%) and ad-1 (6%). Probably right of Bml (2%) (1012, PB). (381). Yellow carotenoids (381). Affects synthesis of neurosporaxanthin (4'-apo-beta'-caroten-4'-oic acid); citations in reference 398. Lesion probably involves the conversion of lycopene to 3,4-dehydrolycopene or the conversion of either torulene or gamma-carotene to neurosporaxanthin (398 and references therein) (Fig. 9). Resembles the orange wild type in young cultures, but color differences become clear with age. Expressed in both conidia and mycelia. Undefined modifiers affect intensity. Fails to complement with many of the al-1 and al-2 albino strains (R.E. Subden, personal communication).	VIL	B
sc	IIIR. Between the centromere and ser-1 (504). Linked to thi-4 (1/280) and spg(0 + + /179); right of acr-2 (3 to 6%) (498, 814). Irregular flat spreading growth with knobby protrusions but no conidia. Mycelium usually appears yellowish rather than orange. Female fertile. Homozygous sc x sc crosses give nonlinear asci (827, 828, 1011). Cell wall analysis (132). Reduced amount of cell wall peptides (1165). Allele R2503 called col-14; allele R2386 called smco-2 (382). For modifier, see mod(sc).	IIIR	B
pan-1	IVR. Between ad-6 (1 to 2%) and cot-1 (2 to 3%) (633, 692, PB). (482). cel, col-1, int, pho-3, and thi-5 all appear to be closely linked in this crowded region. Requires intact pantothenic acid for growth under standard conditions. Able to synthesize both precursors, beta-alanine and pantoyl lactone (1058). Ability to synthesize pantothenic acid from beta-alanine plus pantoyl lactone is demonstrable in vitro but not in vivo unless cultures are aerated (1111, 1113, 1114). Unlike pan-2, pan-1 has no effect on ascospore ripening in heterozygous crosses. Called group A. For alleles see reference 138.	IVR	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
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
nt	VIIR. Between arg-10 (2 to 12%) and sk (7 to 18%) (789). (874) Uses nicotinic acid. May respond also to tryptophan, phenylalanine, tyrosine, quinic acid, and precursors of nicotinic acid or tryptophan, or both, depending on genetic background (448, 760). Best supplemented with nicotinamide and scored as a nic mutant. Probably deficient in tryptophan pyrrolase (tryptophan 2,3-dioxygenase) (Fig. 18), but direct evidence is lacking because tryptophan oxygenase cannot be assayed in Neurospora (368). Kynurenine formamidase levels are normal (368). Pyridine nucleotide levels (111).	VIIR	B