FGSC #2553

Mutant Type

Genus: N

reporting_genes: per-1;pyr-3

species: Neurospora crassa

allele: PBT5;KS43

stock:

glasgow:

mutagen: UV

Depositor: TEJ

Link Group: VR;IVR

MT: A

Species No: 10

gene_back: M

oppmt: 0

trans:

ref1: Johnson 1974. NN 21:19-20, https://doi.org/10.4148/1941-4765.1798

ref2:

site:

country:

ksudc_link: https://digital.lib.k-state.edu/item/neurospora-crassa/fgsc-2553

ksudc_link_html: https://digital.lib.k-state.edu/item/neurospora-crassa/fgsc-2553 ↗

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 Unlike Saccharomyces, no feedback-insensitive CPS+ ACT+ mutants of Neurosporahave been discovered (A. Radford, unpublished data).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
per-1	VR. Right of asp (26%) and at (8 to 14%). Left of ilv(4%) (489, PB) and ts(25%) (527). Perithecial walls are devoid of black pigment when the female parent carries per-1, regardless of genotype of the fertilizing parent (489, 490, 527). Alleles are of two types (490). Type I produces young, completely white perithecia that become pale yellowish after several days, and per-1 ascospores are white (e.g., alleles PBJ1, ABT8, and AR174). Type II produces mature perithecia that are somewhat darker orange with black pigment in the neck, and per-1ascospores are normal black (e.g., alleles 29278, 29-281, and UG1837). Unlike the perithecial wall trait, the ascospore trait shows no maternal effect. Black pigment develops in a ring around the ostiole of type II perithecia, but is pale or lacking in type I perithecia (490). Mosaic perithecia from heterokaryons have been used for a clonal analysis of perithecial development (527, 528). Expression is completely autonomous in ascospores (photographs in reference 529) and at least partially so in the perithecial walls (527-529). Used to test for variegated-type position effect, with negative results (532). White per-1ascospores (type I) germinate without heat shock and are usually killed by hypochlorite or by the 30-min, 60°C treatment used to activate normal ascospores (490, 527). Beaks of perithecia homozygous for allele PBJL (type I) are abnormal, and ascospores are not shot properly (N.B. Raju, personal communication). Type I alleles initially called sw: snow white (527).	VR	B