FGSC #1167

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Mutant Type

Genus: N

reporting_genes: phe-1;inl

species: Neurospora crassa

allele: UA119 89601

stock: 135

glasgow:

mutagen: NA

Depositor: KKJ

Link Group: IL;VR

MT: A

Species No: 10

gene_back: M

oppmt: 0

trans:

ref1: Jha 1965 Neurospora Newslett 7:15-18, https://doi.org/10.4148/1941-4765.2106

ref2: Jha 1969 Neurospora Newsl. 14:3, https://doi.org/10.4148/1941-4765.2025

site:

country:

ksudc_link: https://digital.lib.k-state.edu/item/neurospora-crassa/fgsc-1167

ksudc_link_html: https://digital.lib.k-state.edu/item/neurospora-crassa/fgsc-1167 ↗

Genes

Locus	Cultural Requirements	Link Group	Type
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83201 show slow semicolonial growth in liquid minimal medium at 25°C (641), but look normal on slants (D.D. Perkins, unpublished data).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
phe-1	IL. Right of In(H4250) and suc (<1%). Left of ad-5(816; H.B. Howe, Jr., personal communication). (48) [Duplications from In(H4250) x phe-1 crosses are phe-, unlike duplications from T(39311). The contrary statement on p. 268 of reference 816 is a misprint.] Originally reported to grow on phenylalanine, other aromatic amino acids, leucine, or ethyl acetoacetate, with phenylalanine being most effective; several other acids gave smaller responses (48). Utilization of phenylalanine and other compounds varies for different isolates and on different carbon sources; glycerol or ribose is preferable to sucrose (521-523, 753). Strains carrying allele NM160 do not use phenylalanine but grow well on tyrosine or leucine (816; A.G. De Busk, personal communication), at least with the strains and carbon source used. The mutant phe-1 is inhibited by basic amino acids on low-phenylalanine or leucine medium (48, 521). Growth on beta-labeled leucine or beta-labeled phenylalanine showed that neither compound is converted to the other (45). Called phen-1. Allele NM160 originally called tyr(NM160) (316).	IL	B