FGSC #5266

Mutant Type

Genus: N

reporting_genes: his-2 ad-3A ad-3B nic-2;inl

species: Neurospora crassa

allele: C94 1-112-13 35203 43002 JH319

stock: 74-OR24-1A

glasgow:

mutagen:

Depositor: FJD

Link Group: IR R R R;VR

MT: A

Species No: 10

gene_back: OR

oppmt: 0

trans:

ref1:

ref2:

site:

country:

ksudc_link: https://digital.lib.k-state.edu/item/neurospora-crassa/fgsc-5266

ksudc_link_html: https://digital.lib.k-state.edu/item/neurospora-crassa/fgsc-5266 ↗

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
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
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
ad-3A	IR. Between his-3 (1 to 2%) and ad-3B (0.1 to 0.7%) (271). Right of ure-4 (78). (482) Requires adenine or hypoxanthine (682). Blocked in interconversion of CAIR plus aspartate to SAICAR (348) (Fig. 8). Produces purple pigment, permitting direct visual selection (276, 682); see the ad-3B entry. Reduced interallelic fertility (407). No interallelic complementation (267; F.J. de Serres, personal communication). ad-3A and ad-3B are two genetically and functionally distinct loci separated by a short but functionally complex region of unknown but essential function (271, 407). They have been used intensively for quantitative genetic and molecular studies of mutation (for a review, see reference 35). Either forward mutation (e.g., reference 277) or reverse mutation (e.g., reference 772) can be measured precisely; the former is detected visually by purple pigment. Purple pigment has also been used to assess the effect of histidine and tryptophan on purine nucleotide synthesis (786). Alleles N23 and N24 have been used as mutagen testers. N23 reverts with agents that cause base pair substitutions; N24 reverts with agents that cause frameshifts (772). SK(ad-3A) is at or near ad-3A and may be a cryptic ad-3A allele. Does not require adenine. In SK(ad-3A)x ad-3Acrosses, the ad-3A progeny die; possibly SK(ad-3A) mutants fail to make enough adenine to support their growth (251). Translocations Y155M64 ad-3A (272; PB) and Y112M15 ad-3A(413) each have one breakpoint that is inseparable from ad-3A. Called complementation group A (264). "A" in the locus symbol does not refer to mating type.	IR	B
his-2	IR. Right of T(AR190) and un-2 (<1%). Left of the T(AR173) right breakpoint and of nuc-1 (<1%) (172, 670, 808). (434)Requires histidine (434). Affects adenosine 5'-triphosphate phosphoribosylpyrophosphate pyrophosphorylase (16) (Fig. 14). Intralocus complementation (162). Recombination between his-2 alleles is controlled by rec-3(173); it is not affected by rec-1 (172). Initial his-2 allele called C94.	IR	B