FGSC #7272

Mutant Type

Genus: N

reporting_genes: pyr-3;trp-3;am132 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-7272

ksudc_link_html: https://digital.lib.k-state.edu/item/neurospora-crassa/fgsc-7272 ↗

Genes

Locus	Cultural Requirements	Link Group	Type
pyr-3	IVR. Right of the T(NM152) left breakpoint and of T(S1229); hence, right of arg-14. Left of his-5 (1%) (238, 808). (482) Requires uracil or other pyrimidine (683). Growth inhibited by purine nucleosides and nucleotides (825). Structural gene for pyrimidine-specific carbamyl phosphate synthase (CPS) and aspartate carbamyl transferase (ACT; also abbreviated ATC) (456, 850) (Fig. 20). Mutants may lack either or both activities, e.g., those carrying alleles KS43 (CPS+ ACT-), KS20 (CPS- ACT+), and KS11 (CPS- ACT-) (1140). Unlike Saccharomyces, no feedback-insensitive CPS+ ACT+ mutants of Neurosporahave been discovered (A. Radford, unpublished data). Some mutants have kinetically altered aspartate carbamyl transferase (456, 880). Used extensively for studies of channeling and relation of gene structure to the two enzyme activities (236). Normally, carbamyl phosphate produced by pyr-3+ is used solely for pyrimidine synthesis, and carbamyl phosphate produced by arg-2+ and arg-3+ is used for arginine synthesis, the enzymes being in different organelles; however, a deficiency of the next enzyme in either pathway permits overflow of carbamyl phosphate into the other pathway (reviewed in reference 236). Hence, CPS- ACT+ alleles are suppressed by arg-12s (246), and CPS+' ACT- alleles can be selected as suppressors of arg-2and arg-3 (658, 887, and references therein). Some of the CPS+ ACT- mutations, called pyr-su-arg, suppress the arginine requirement but retain enough aspartate carbamyl transferase activity that they have no detectable pyrimidine requirement (877, 881). arg-13, arg-4, arg-5, arg-6, and am partly suppress CPS- ATC+ alleles (see reference 660). Fine-structure map (851, 1050). Fertility of interallelic crosses is variable and often very poor (658). Complementation between CPS- ACT+ and CPS+ ACT- mutants (246) and between some pairs of CPS+ ACT- mutants is good; otherwise, complementation is poor (849, 1159). Complementation maps (658, 849, 877, 1159). Mutational analysis (852). Direction of translation, based on enzyme types of polar mutants, is from CPS to ACT (850). Allele 37815(t) is heat sensitive (34°C versus 25 C) (68). Allele 1298 is C02 remediable (191, 192). Strain KS12, a pyr-1 pyr-3 double mutant, was originally called pyr-5 (see reference 346). The different classes of pyr-3 alleles have been called M (CPS-P-less), N (ACT-less), and MN (lacks both activities).	IVR	B
trp-3	IIR. Right of fl (2 to 6%). Left of rip-1 (9%) and un-5(10%) (816, PB). (1166). Uses tryptophan (685); strains carrying some alleles also use indole (4). Structural gene for tryptophan synthetase (1167), called tryptophan desmolase in early literature. Tryptophan synthetase catalyzes three reactions: indoleglycerol-phosphate -> tryptophan, indole tryptophan, and indoleglycerol-phosphate <-> indole (Fig. 11). In Neurospora, all three reactions are catalyzed by a single protein, which is specified by a single gene (645, 1167). Mutants lack indoleglycerol-phosphate -> tryptophan activity but differ with respect to the other activities; e.g., strains carrying trp-3 allele (td141 are blocked in indoleglycerol-phosphate utilization but can use indole; trp-3 (td100) can synthesize indole but not convert it to tryptophan; trp-3 (td140) lacks all three activities. (See references 582 and 1049 for citations and characteristics of other mutants.) Used extensively for studies of gene structure in relation to enzymatic activity (257, 582 and references therein, 1167). The active enzyme is a homooligomer (645) thought to have two domains (644 and references therein). Biochemical studies of complementation between alleles: in vivo (582, 583) and in vitro (1048 and references therein). Complementation maps (4, 5, 9 and references therein, 582). Fine-structure maps (5, 540, 582, 1049). Reviewed as example of gene fusion (218). trp-3 mutant C83 provided the first proved example in Neurospora of gene-controlled loss of enzyme activity (685); trp-3 mutant S1952 provided the first example of allele-specific suppression restoring functional wild-type-like enzyme (1166). Allele td140 is supersuppressible (954, 955). Certain classes of trp-3mutants are osmotic remediable (583). Called td and tryp-3.	IIR	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
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
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
am132			B