FGSC #6036

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Reporting Genes: nit-2;inl

Species: crassa

Allele: KGP0220 37401

Alternate Strain Number: 336

Mutagen: UV

Depositor: GAM

Linkage Group: IL;VR

Mating Type: A

Species Number: 10

Genetic Background: M

Deposit Sheet ↗

Genes

Locus	Cultural Requirements	Link Group	Type
nit-2	IL. Right of the T(39311) left breakpoint and of un-5(2%). Left of In(OY323) and leu-3 (12 to 18%) (57, 808, 816, PB). (335, 1135) Cannot use nitrate, nitrite, purines, or most amino acids as a nitrogen source but will grow on ammonia, glutamine, or glutamate. nit-2+ is a major nitrogen control gene and mediates nitrogen catabolite repression. The nit-2 mutant is missing (or has severely reduced levels of) nitrate reductase, nitrite reductase, uricase, xanthine dehydrogenase, allantoinase, allantoicase, L-amino acid oxidase, general amino acid permease, extracellular protease, and an intracellular neutral phenylmethylsulfonyl fluoride-sensitive protease (227, 324, 441, 872, 1001, and references therein). Also affects levels of glutamate dehydrogenases (226) and uptake of uracil and uridine (128). Prevents leaky growth of the mutant am on minimal medium (155). The product of the nit-2gene has been tentatively identified as a nuclear DNA-binding protein, whose affinity for DNA is reduced in the presence of glutamine (433). Allele K31 (called pink) originated in N. sitophila and was introgressed into N. crassa (335); protein product of K31 may show altered mobility (433). Recombination within the nit-2 locus is subject to regulation by rec-1 (157). Heterozygosity for closely linked ss reduces recombination within nit-2 (161). Called amr: ammonium regulation in reference 872.	IL	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