FGSC #4194

Mutant Type

Genus: N

reporting_genes: uvs-3;trp-4 pan-1

species: Neurospora crassa

allele: ALS11 Y2198 5531

stock: M938 A

glasgow:

mutagen:

Depositor: EK

Link Group: IVLR

MT: A

Species No: 10

gene_back:

oppmt: 4195

trans:

ref1: Kafer 1982. Neurospora Newsl. 29:41-44, https://doi.org/10.4148/1941-4765.1645

ref2:

site:

country:

ksudc_link: https://digital.lib.k-state.edu/item/neurospora-crassa/fgsc-4194

ksudc_link_html: https://digital.lib.k-state.edu/item/neurospora-crassa/fgsc-4194 ↗

Genes

Locus	Cultural Requirements	Link Group	Type
pan-1	IVR. Between ad-6 (1 to 2%) and cot-1 (2 to 3%) (633, 692, PB). (482). cel, col-1, int, pho-3, and thi-5 all appear to be closely linked in this crowded region. Requires intact pantothenic acid for growth under standard conditions. Able to synthesize both precursors, beta-alanine and pantoyl lactone (1058). Ability to synthesize pantothenic acid from beta-alanine plus pantoyl lactone is demonstrable in vitro but not in vivo unless cultures are aerated (1111, 1113, 1114). Unlike pan-2, pan-1 has no effect on ascospore ripening in heterozygous crosses. Called group A. For alleles see reference 138.	IVR	B
trp-4	IVR. Between his-5 (3 to 7%) and leu-2 (1 to 2%) (633, 991). (47). Uses tryptophan or indole (750). Deficient in anthranilate phosphoribosyl transferase (1126) (Fig. 11). Scorable by blue fluorescence (anthranilate) in medium under long-wave UV after 2 to 5 days of growth on minimal medium plus indole (10 µg /ml), 34°C. Initial stocks of the first trp-4 mutant were inhibited by suboptimal concentrations of tryptophan (750), but derivatives have been obtained that are free of this problem (909).	IVR	B
uvs-3	VL. Linked to cys-10 (3 to 7%), probably to the left (538, 932).Allele ALS11 is sensitive to UV (273, 932, 933), ionizing radiation (537, 933, 940), methyl methane sulfonate (536), nitrosoguanidine (509, 933), mitomycin C (195, 537), histidine (932), and 4-nitroquinoline 1-oxide and ICR-170 (509). Reverts spontaneously (932). No UV-induced mutation (273). For mutation induction by other agents, see references 509 and 940. Increased spontaneous mutation (275, 537). Dimer excision delayed and at reduced rate (1164). Defective photoreactivation in vivo, but photoreactivation enzyme functions in vitro (934). Defective in extracellular nuclease, giving reduced halo around colonies on DNA agar (538). Apparently deficient in proteolytic conversion of nuclease precursor to active intra- and extracellular deoxyribonucleases, but this effect could be indirect (360). Increased stability of CPS(Pyr) and ACT activities in vitro also suggests that protease activity may be reduced in uvs-3 mutants (882). Causes increased duplication instability (mitotic recombination or deletion or both) (932). Conidial viability is low (275, 932). Double mutant upr-1;uvs-3 is much more sensitive to UV than is either single mutant (1095). Double mutant uvs-3;uvs-6 is inviable (506). Homozygous barren, with block before karyogamy (860, 932). Shows high level of repair of genetic damage without induction in rescuing a heterokaryotic component that carries potentially lethal mutagen-induced damage (1022). Probable allele FKO16, isolated as halo mutation nuh-4, resembles uvs-3 allele ALS11 but is less extreme in some properties, e.g., it shows better conidial survival (538; see reference 537).	VL	B