FGSC #4193

Mutant Type

Genus: N

reporting_genes: uvs-3;ylo-1 pan-2

species: Neurospora crassa

allele: ALS11;Y30539y B5(Y154M64)

stock: M935 a

glasgow:

mutagen:

Depositor: EK

Link Group: IVL;VI-CR

MT: a

Species No: 10

gene_back:

oppmt: 0

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-4193

ksudc_link_html: https://digital.lib.k-state.edu/item/neurospora-crassa/fgsc-4193 ↗

Genes

Locus	Cultural Requirements	Link Group	Type
pan-2	VIR. Right of rib-1 (<1 to 3%). Left of del (6%) and trp-2(11%) (140, 141, 143, 818, PB). Unable to convert ketovaline to ketopantoic acid (138, 140, 141). Used in major studies of intralocus recombination and complementation (140-143). pan-2ascospores remain white or pale if the crossing medium is not supplemented, even when the protoperithecial parent is pan-2+. Asci in which gene conversion has occurred at pan-2 can thus be recognized and isolated (1072, 1073); photographs (1072). For good recovery of pan-2progeny, crossing media should be supplemented with pantothenic acid (10 µg/ml) even when the protoperithecial parent is pan+. Called group B.	VIR	B
ylo-1	VIL. Between cys-1 (8%) and ad-1 (6%). Probably right of Bml (2%) (1012, PB). (381). Yellow carotenoids (381). Affects synthesis of neurosporaxanthin (4'-apo-beta'-caroten-4'-oic acid); citations in reference 398. Lesion probably involves the conversion of lycopene to 3,4-dehydrolycopene or the conversion of either torulene or gamma-carotene to neurosporaxanthin (398 and references therein) (Fig. 9). Resembles the orange wild type in young cultures, but color differences become clear with age. Expressed in both conidia and mycelia. Undefined modifiers affect intensity. Fails to complement with many of the al-1 and al-2 albino strains (R.E. Subden, personal communication).	VIL	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