FGSC #7278

Mutant Type

Genus: N

reporting_genes: arg-12;am inl inv mei-2

species: Neurospora crassa

allele:

stock:

glasgow:

mutagen:

Depositor: RLM

Link Group:

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-7278

ksudc_link_html: https://digital.lib.k-state.edu/item/neurospora-crassa/fgsc-7278 ↗

Genes

Locus	Cultural Requirements	Link Group	Type
arg-12	Uses arginine or citrulline.	IIR	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83201 show slow semicolonial growth in liquid minimal medium at 25°C (641), but look normal on slants (D.D. Perkins, unpublished data).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
inv	VR. Right of pab-2 (3%) and ro-4 (5 to 8%), Left of asn (4 to 9%) (918, PB).Unable to use sucrose as a carbon source. Grows well on glucose or fructose and fairly well on Casamino Acids or yeast extract. Invertase structural gene; invertase deficient and uninducible by normal inducers. Makes cross-reacting material (919). Invertase is also affected by cot-2, q.v.	VR	B
mei-2	VR. Linked near inl (995). Between al-3 (20 and his-6(A.L. Schroeder, personal communication). Meiotic divisions occur, and many ascospor are produced, but many are inviable and white. Crosses heterozygous or homozygous for Mei-2 give extensive nondisjunction of all linkage groups (995). Chromosome pairing much reduced (B.C. Lu, cited in reference 995). Sensitive to methyl methane sulfonate, histidine, and gamma rays (939). Dominant in the original strain (995), but progeny show incomplete penetrance (939).	VR	B
am	VR. Right of ure-2 (2%) and sp (4 to 8%). Left of gul-1(<<1%) and ace-5(<1%) (122, 570, 579, 998). (R.W. Barratt, (cited in reference 1036) Structural gene for nicotinamide adenine dinucleotide phosphate (NADP)-glutamate dehydrogenase (336) (see Fig. 19), for which a complete 452-residue amino acid sequence has been obtained (465). Requires a source of alpha-amino nitrogen for growth, alanine being a good supplement (e.g., reference 997). Readily scorable at 25 C; leaky at 34°C (42). Leaky growth and adaptation on minimal medium are prevented by 0.02 M glycine (782, 783) or by en(am)-1, en(am)-2, or nit-2, q.v. The ammutants show abnormal regulation of reduced nicotinamide adenine dinucleotide (NADH)-glutamate dehydrogenase and are synergistic with nit-2 in this effect (226). Some am alleles (e.g., RU1) suppress the pyrimidine requirement caused by pyr-3 (CPS- ACT+) mutations (1137). Used for the first demonstration of complementation between alleles in vivo (344) (simultaneous with independent demonstration with ad-4). In vitro complementation (342). Used for studies of complementation mechanism (199, 200, 1120). Used for fine-structure mapping (337, 338). Control of intralocus recombination by rec-3(996-998). Used to study colinearity of the gene and gene product, internal suppressors (105, 340, 465), and the action of supersuppressors (954, 955). The functional defects in several mutant enzymes with single amino acid replacements have been defined: am1 mutant enzymes fail to bind NADPH (1120); am2, am3, am19, am130, and am131 enzymes are stabilized in the inactive conformational form (30, 200, 336, 556, 1044), and all are complementable by am1; am14 is osmotically reparable and is thought to have unstable quaternary structure (340). Used in a study showing glutamine to have a role as corepressor of uricase synthesis (1118). Used to study nitrogen assimilation and metabolism (503) and nitrogen metabolite repression (186, 291). Efficient procedure for selecting new am mutants (551). Spectrum of ultraviolet irradiation (UV)- and nitrous acid-induced mutants (554). Allele am17 has a chain-terminating codon of either the amber or ochre type at residue 313 of glutamate dehydrogenase, based on amino acid replacements in revertants and by ssu-1 (956). Allele 6 is a frameshift mutation with an insertion in the Ser5 codon (985). Allele 126 is highly unstable (553). Allele 132 is a deletion (1162). The am+ gene has been cloned in Escherichia coli(J.R.S. Fincham, personal communication) and transformed back into Neurospora (J.A. Kinsey, personal communication).	VR	B