FGSC #4133

Mutant Type

Genus: N

reporting_genes: cyh-2 al-3 inl pab-2

species: Neurospora crassa

allele: KH53(r) RP100 83201(t) H193

stock: M1011 A

glasgow:

mutagen:

Depositor: EK

Link Group: VCR

MT: A

Species No: 10

gene_back:

oppmt: 0

trans:

ref1: Kafer 1982. Neurospora Newsl. 29:41-44, https://doi.org/10.4148/1941-4765.1645

ref2:

site:

country:

ksudc_link: https://digital.lib.k-state.edu/item/neurospora-crassa/fgsc-4133

ksudc_link_html: https://digital.lib.k-state.edu/item/neurospora-crassa/fgsc-4133 ↗

Genes

Locus	Cultural Requirements	Link Group	Type
cyh-1	IR. Right of nit-1 (6%). Left of T(STL76) and al-2 (8 to 13%) (496, 797, 808).Resistant to cycloheximide (496, 748). Resistance is recessive in duplications (1090). Dominance reported in forced heterokaryons (496, 748) may have been due to skewed nuclear ratios (1090). Protein synthesis on ribosomes of the mutant cyh-1 proceeds in the presence of cycloheximide in a cell-free system (834). Readily scored on slants with 10 µg of cycloheximide per ml autoclaved in the medium. Excellent as a marker and valuable for selecting somatic recombinants or deletions in heterozygous duplications (748, 1091). Used to show that the cycloheximide-induced phase shift of the circadian clock involves protein synthesis (738). Called act-1: actidione resistant-1.	IR	B
cyh-1	IR. Right of nit-1 (6%). Left of T(STL76) and al-2 (8 to 13%) (496, 797, 808).Resistant to cycloheximide (496, 748). Resistance is recessive in duplications (1090). Dominance reported in forced heterokaryons (496, 748) may have been due to skewed nuclear ratios (1090). Protein synthesis on ribosomes of the mutant cyh-1 proceeds in the presence of cycloheximide in a cell-free system (834). Readily scored on slants with 10 µg of cycloheximide per ml autoclaved in the medium. Excellent as a marker and valuable for selecting somatic recombinants or deletions in heterozygous duplications (748, 1091). Used to show that the cycloheximide-induced phase shift of the circadian clock involves protein synthesis (738). Called act-1: actidione resistant-1.	IR	B
cyh-2	VR. Right of lys-2 (<1%). Left of leu-5 (<1 to 2%) and sp(2 to 9%) (496, 818, PB). Resistant to cycloheximide (496, 748). Protein synthesis on mutant ribosomes proceeds in the presence of cycloheximide in a cell-free system (834). Excellent marker. Readily scored on slants with 10 µg of cycloheximide per ml autoclaved in the medium or with 1 µg added after autoclaving. Resistance in heterokaryons has been reported to be dominant (496, 626) or recessive (939); it may depend on nuclear ratios or media. Used in mutagenicity test systems (626). Used to show that the cycloheximide-induced phase shift of the circadian clock involves protein synthesis (738). Double mutant cyh-1;cyh-2grows slowly and is much more insensitive to cycloheximide than either single mutant (496).	VR	B
cyh-2	VR. Right of lys-2 (<1%). Left of leu-5 (<1 to 2%) and sp(2 to 9%) (496, 818, PB). Resistant to cycloheximide (496, 748). Protein synthesis on mutant ribosomes proceeds in the presence of cycloheximide in a cell-free system (834). Excellent marker. Readily scored on slants with 10 µg of cycloheximide per ml autoclaved in the medium or with 1 µg added after autoclaving. Resistance in heterokaryons has been reported to be dominant (496, 626) or recessive (939); it may depend on nuclear ratios or media. Used in mutagenicity test systems (626). Used to show that the cycloheximide-induced phase shift of the circadian clock involves protein synthesis (738). Double mutant cyh-1;cyh-2grows slowly and is much more insensitive to cycloheximide than either single mutant (496).	VR	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
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
pab-2	VR. Right of ad-7 (8%). Left of inv (3%) and asn (1 to 15%). Linked to ro-4(0/407) (156, 816, 818, 918, 1036). (47) Requires p-aminobenzoic acid (1182) (Fig. 11). Allele 71301 called pab-3(1182); shown to be allelic by Drake (289).	VR	B
pab-2	VR. Right of ad-7 (8%). Left of inv (3%) and asn (1 to 15%). Linked to ro-4(0/407) (156, 816, 818, 918, 1036). (47) Requires p-aminobenzoic acid (1182) (Fig. 11). Allele 71301 called pab-3(1182); shown to be allelic by Drake (289).	VR	B