FGSC #7257

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Mutant Type

Genus: N

reporting_genes: nic-3 oli;inl inv mei-2

species: Neurospora crassa

allele:

stock:

glasgow:

mutagen:

Depositor: RLM

Link Group:

MT: a

Species No: 10

gene_back:

oppmt: 0

trans:

ref1:

ref2:

site:

country:

ksudc_link: https://digital.lib.k-state.edu/item/neurospora-crassa/fgsc-7257

ksudc_link_html: https://digital.lib.k-state.edu/item/neurospora-crassa/fgsc-7257 ↗

Genes

Locus	Cultural Requirements	Link Group	Type
inv	VR. Right of pab-2 (3%) and ro-4 (5 to 8%), Left of asn (4 to 9%) (918, PB).Unable to use sucrose as a carbon source. Grows well on glucose or fructose and fairly well on Casamino Acids or yeast extract. Invertase structural gene; invertase deficient and uninducible by normal inducers. Makes cross-reacting material (919). Invertase is also affected by cot-2, q.v.	VR	B
mei-2	VR. Linked near inl (995). Between al-3 (20 and his-6(A.L. Schroeder, personal communication). Meiotic divisions occur, and many ascospor are produced, but many are inviable and white. Crosses heterozygous or homozygous for Mei-2 give extensive nondisjunction of all linkage groups (995). Chromosome pairing much reduced (B.C. Lu, cited in reference 995). Sensitive to methyl methane sulfonate, histidine, and gamma rays (939). Dominant in the original strain (995), but progeny show incomplete penetrance (939).	VR	B
nic-3	VIIL. Right of spco-4 (1%) and do (3%). Left of thi-3 (9 to 27%) and csp-2 (16 to 22%) (539, 812, 816, PB). (M.K. Allen, cited in references 718 and 789) Uses nicotinic acid, nicotinamide, 3-hydroxyanthranilic acid, 3-hydroxykynurenine, or high concentrations of quinolinic acid (96, 1168). Accumulates alpha-N-acetylkynurenine; blocked in conversion of kynurenine to 3-hydroxykynurenine (1168) (Fig. 18). Pyridine nucleotide levels (111). Pathway from tryptophan to nicotinic mononucleotide, showing sites of gene action (96, 100, 368, 1168). The enzymatic reactions between 3-hydroxyanthranilate and nicotinic mononucleotide have not been demonstrated directly in Neurospora.	VIIL	B
oli	VIIR. Between met-9 (8 to 24%) and arg-11 (3 to 16%) (960). Linked to frq-1 (<2%) and possibly allelic (282, 283). (959) Resistant to oligomycin. Defective in energy transduction (313). Structural gene for dicyclohexylcarbodiimide-binding proteolipid (subunit 9) of F0 portion of mitochondrial adenosine triphosphate synthetase (958). The amino acid sequence (81 residues) (959) shows extensive homology with the corresponding proteolipid in yeast, in which, in contrast to Neurospora, it is the product of a mitochondrial gene (960, 1109). Specific single amino acid substitutions have been identified for three mutants (959). oli mutants are selected effectively by using double mutant azs; has (called ANT-1), which is deficient in both salicyl hydroxamic acid-sensitive and azide-sensitive alternate oxidase pathways. Scored on 5 µg of oligomycin per ml of liquid medium, 3 days, 30°C (312). Altered period of circadian rhythm cosegregates and reverts with oli (282, 283).	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