FGSC #3757

Mutant Type

Genus: N

reporting_genes: lys(60C);inl

species: Neurospora crassa

allele: 60C(t);89601

stock: 60C

glasgow:

mutagen: UV

Depositor: DRS

Link Group: I;VR

MT: a

Species No: 10

gene_back: M

oppmt: 0

trans:

ref1: Stadler 1981 NN 28:18, https://doi.org/10.4148/1941-4765.1660

ref2:

site:

country:

ksudc_link: https://digital.lib.k-state.edu/item/neurospora-crassa/fgsc-3757

ksudc_link_html: https://digital.lib.k-state.edu/item/neurospora-crassa/fgsc-3757 ↗

Genes

Locus	Cultural Requirements	Link Group	Type
lys(60C)	All lysine auxotrophs are inhibited competitively by arginine (287, 288). Resistance to arginine is conferred on lys-1 mutants by a presumed transport mutation argR, q.v. See the arg entry for medium that provides both lysine and arginine requirements. Lysine biosynthesis is by the alpha-aminoadipate pathway in Neurospora and other higher fungi (see reference 1103) (Fig. 16). Complex interactions between lys, pyr, and argmutations have been described (485). Enzymes of lysine biosynthesis are derepressed coordinately with those of arginine, histidine, and tryptophan (1131). See cpc-1.Biosynthetic pathway of lysine, showing sites of gene action of lys-4and lys-5and probable sites of lys-2 and lys-3 gene action (119, 400, 464, 762, 1087). alpha-amino-epsilon-hydroxycaproic acid can be converted to alpha-aminoadipate semialdehyde (1178), but apparently is not an intermediate.		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