FGSC #2715

Mutant Type

Genus: N

reporting_genes: Not available; pan-2;cot-1;al-2;uvs-3

species: Neurospora crassa

allele: Y387-15.7;C102(t);Y112M38;ALS11

stock: 74-OR266-20a

glasgow:

mutagen:

Depositor: FJD

Link Group: VIR;IVR;IR;IVL

MT: a

Species No: 10

gene_back:

oppmt: 2714

trans:

ref1:

ref2:

site:

country:

ksudc_link: https://digital.lib.k-state.edu/item/neurospora-crassa/fgsc-2715

ksudc_link_html: https://digital.lib.k-state.edu/item/neurospora-crassa/fgsc-2715 ↗

Genes

Locus	Cultural Requirements	Link Group	Type
al-2	IR. Right of os-5 (<1%) and T(STL76). Left of arg-6(1%) and al-1 (797, 802, 808, 816, 818). Included in duplications from Tp(T54M94), confirming location left of arg-6(808). (482) Carotenoids absent or abnormal, but steroids produced (398). Blocked in microsomal fraction and defective in phytoene synthetase (445), a particulate enzyme (445 and references cited therein) (Fig. 9). Tracer experiments indicate a lesion between prephytoene pyrophosphate and phytoene (572). Alleles include those resulting in white and pale rose-white, e.g., 15300 and Y254MI65 (1042), and purple, e.g., MN58a (154). For complementation, see references 500 and 1041. Fine-structure mapping (500, 1042) needs reevaluation because of new information on the location of the arg-6 marker (797).	IR	B
cot-1	IVR. Between pan-1 (2%) and his-4 (1 to 6%) (692, 812, 816). Extremely colonial at 34°C, but completely normal growth, morphology, and fertility at 25°C and below. Linear growth is maximum at 24°C (374). Becomes colonial at 32°C; colonies from ascospores or conidia are viable and continue to grow slowly with dense branching, but do not conidiate. They quickly resume normal growth when shifted to a permissive temperature (692, 1068). Recessive in duplications (808); apparent dominance in heterokaryons (374) may have resulted from a shift in nuclear ratios. Used in studies of septation and branching (202), growth-inhibiting mucopolysaccharide (878, 879), and sulfate transport (641). Cell wall analysis (374). Growth is stimulated by lysine or arginine (0.1 mM) on glucose media at high temperatures (615). Because of high viability and tightly restricted growth at restrictive temperatures and normality at 25°C, cot-1 mutants have valuable technical applications. For example, crosses homozygous for cot-1 have been used in combination with sorbose for experiments with rec genes, where high-density ascospore platings are required for precise quantitative analysis of intralocus recombination (e.g., references 165, 997, and 1070). In another application, when shifted up after initial growth at the permissive low temperature, cot-1hyphae assume a "bottle brush" appearance with small side branches (692). This has been used to select uvs mutants by subsurface survival on UV-irradiated plates containing p-aminobenzoic acid (938; D.E.A. Catcheside, personal communication). cot-1 conidia or ascospores from cot-1 x cot-1crosses are used for replication in a protocol involving transfer by filter paper (615). For suppressors of cot-1, see gul.	IVR	B
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
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