FGSC #6023

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Reporting Genes: ssu-1;nit-3;inl

Species: crassa

Allele: WRN33;KGP1211;37401

Alternate Strain Number: 825

Mutagen: UV

Depositor: GAM

Linkage Group: VIIR;IVR;VR

Mating Type: a

Species Number: 10

Genetic Background: M

ref1: Perrine and Marzluf 1986 Current Genetics 10:677, https://doi.org/10.1007/bf00410916

Deposit Sheet ↗

Genes

Locus	Cultural Requirements	Link Group	Type
ssu-1	VIIR. Right of met-7 (14%). Left of nt (23%) and of missense suppressor su(trp-3td201)-1 (10%) (954). Allele WRN33 selected (953) as suppressor of nonsense mutation am(17), which may be either amber or ochre but cannot be UGA (956). Inserts tyrosine in the site where the wild type has glutamate (956). Used to identify suppressible alleles of aro(p), trp-1, trp-2, trp-3 (953, 144, 183), and ad-3B (749). Although perhaps the most efficient of known ssumutations, ssu-1 restores only about 20% of the wild-type amount of normal glutamate dehydrogenase in the double mutant with am allele (17) (reference 956).	VIIR	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
nit-3	IVR. Between met-5 (15%) and pyr-2 (2 to 9%) (1000, PB). (453) Cannot use nitrate as a nitrogen source, but uses nitrite, ammonia, hypoxanthine, or amino acids (28, 999). Structural gene for NADPH nitrate reductase (28) (Fig. 19). Allele 14789 apparently codes for an altered enzyme that cannot catalyze the whole electron transport sequence from NADPH to N03-, but can catalyze the terminal portion of this sequence, providing that a suitable electron donor (reduced viologen dye) is provided (999). See reference 198 for a model of interaction of nit-1 and nit-3 gene products. For regulation, see references 226, 999, and 1000. The nit-3+ gene has been cloned and is expressed in Escherichia coli (989).	IVR	B