FGSC #5156

Mutant Type

Genus: N

reporting_genes: acr-2;leu-1;ylo-1;cys-10;cyh-2 inl pab-2

species: Neurospora crassa

allele: KH5(r) 33757 Y30539y 39816 KH53(r) 83201t H193

stock: M2068

glasgow:

mutagen:

Depositor: EK

Link Group: III;IL;VIL;IVL;VR VR VR

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-5156

ksudc_link_html: https://digital.lib.k-state.edu/item/neurospora-crassa/fgsc-5156 ↗

Genes

Locus	Cultural Requirements	Link Group	Type
leu-1	IIIR. Between ad-4 (1 to 5%) and his-7 (8%) (219, 578, 815, 1052). (868)Requires leucine (867, 868). Lacks beta-isopropylmalate dehydrogenase (426) (Fig. 15). Accumulates alpha-isopropylmalate and beta-isopropylmalate (427). Synthesis of the enzyme also requires the function of regulatory gene leu-3+ and the presence of alpha-isopropylmalate, which acts as inducer (427). Resistant to aminotriazole (D. D. Perkins, unpublished data). Female sterile (O. M. Mylyk, personal communication). Used to study reversion and competition in heterokaryons (901).	IIIR	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
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
cys-10	IVL. Left of acon-3 (1 to 6%), ace-4 (19 to 33%), and cut (28 to 37%) (578, PB). (721) Uses cysteine, cystathionine, homocysteine, or methionine, with a slight response to thiosulfate (469, 596, 721); however, E. Kafer (personal communication) found good growth on thiosulfate. Growth is better on casein hydrolysate than on methionine (D.D. Perkins, unpublished data). cys-10 chol-1double mutants grow better on methionine alone than on methionine plus choline (721). Lacks sulfite reductase, as do cys-2 and cys-4mutants (596). Formerly called met-4; see reference 721.	IVL	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
acr-2	III. Linked to thi-4 (0/286). Left of sc (3 to 6%) and spg (1 to 11%) (498, 816). acr-2 has been shown left of the centromere on published maps but without direct evidence. acr-2and trp-1 (on IIIR) cosegregated at the second division in 1 of 13 asci (H.B. Howe, Jr., personal communication), which would favor a right arm location. Resistant to acriflavine (494, 495); also resistant to 3-amino-1,2,4-triazole (seven alleles tested) (494). Resistance is probably dominant (heterokaryon tests) (498). Not resistant to malachite green. An excellent stable marker, fully fertile, with unambiguous scoring. Sizable inocula should be used to avoid false-negative tests. Use acriflavine at 50 µg /ml in minimal agar medium (816) (higher concentrations may be used) and aminotriazole at 0.5 mg/ml; both added before autoclaving.	III	B
ylo-1	VIL. Between cys-1 (8%) and ad-1 (6%). Probably right of Bml (2%) (1012, PB). (381). Yellow carotenoids (381). Affects synthesis of neurosporaxanthin (4'-apo-beta'-caroten-4'-oic acid); citations in reference 398. Lesion probably involves the conversion of lycopene to 3,4-dehydrolycopene or the conversion of either torulene or gamma-carotene to neurosporaxanthin (398 and references therein) (Fig. 9). Resembles the orange wild type in young cultures, but color differences become clear with age. Expressed in both conidia and mycelia. Undefined modifiers affect intensity. Fails to complement with many of the al-1 and al-2 albino strains (R.E. Subden, personal communication).	VIL	B