FGSC #1325

Mutant Type

Genus: N

reporting_genes: oxD met-1;inl

species: Neurospora crassa

allele: 8 38706;89601

stock:

glasgow:

mutagen:

Depositor: NHH

Link Group: IVR IVR;VR

MT: A

Species No: 10

gene_back:

oppmt: 889

trans:

ref1: J. Biol. Chem. 237:138 1962, https://doi.org/10.1016/S0021-9258(18)81376-X

ref2:

site:

country:

ksudc_link: https://digital.lib.k-state.edu/item/neurospora-crassa/fgsc-1325

ksudc_link_html: https://digital.lib.k-state.edu/item/neurospora-crassa/fgsc-1325 ↗

Genes

Locus	Cultural Requirements	Link Group	Type
oxD	IVR. Between the T(S1229) breakpoints; hence, right of pdx-1(0/55 asci). Left of met-1 (3%) (55, 768, 808). Lacks D-amino acid oxidase. Unable to use D-methionine to satisfy the growth requirement of the mutant met-1. Increased sensitivity to toxic effects Of D-phenylalanine and D-tyrosine. Unable to use D-methionine as the sole sulfur source (768). Resistant to D-ethionine (477). Strains carrying allele oxD1 are cysteine auxotrophs, probably owing to a closely linked coincident lesion (768); see cys-15.	IVR	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
met-1	IVR. Right of oxD (3%) and the T(S1229) left breakpoint. Left of col-4 (4%) (55, 158, 718, 768, 808). Uses methionine but not homocysteine (469) (Fig. 17). Lacks methylene tetrahydrofolate reductase and, thus, lacks the coenzyme needed for transmethylating homocysteine (124, 963, 964). A report that the mutant met-1 also lacks cystathionine-gamma-synthase (547) proved incorrect; the error resulted because methyl tetrahydrofolate is an essential activator of cystathionine-gamma-synthase (965). Methylene tetrahydrofolate reductase is feedback-inhibited by S-adenosylmethionine (124). Used in heteroallelic duplications from T(S1229) to assay mitotic recombination (56).	IVR	B