FGSC #7880

Add to Cart

Reporting Genes: sn cr-1 cyh-1;ad-2;uvs-2;trp-2

Species: crassa

Alternate Strain Number: 7

Depositor: DRS

Linkage Group: IC R R;IIIR;IVR;VIR

Mating Type: A

Species Number: 10

ref1: Stadler and Macleod 1984. Mutat. Res. 127:39-47, https://doi.org/10.1016/0027-5107(84)90138-6

Deposit Sheet ↗

Genes

Locus	Cultural Requirements	Link Group	Type
sn	I. Right of T(39311) and arg-3 (1 to 6%). Left of T(AR173) and his-2 (<1 to 12%) (174, 808). (687) Spreading colonial growth with good conidiation. Linear growth is less than 1/10 that of the wild type (19). Detectable immediately after ascospore germination by hyphal patterns which suggested the name (688). Abnormal microfilaments (19). Contains actin-like protein (20). Said not to exhibit cytoplasmic streaming (18). Meiosis and ascospore formation are normal in homozygous sn x sn crosses (N.B. Raju, personal communication). Good female fertility. Morphology similar to that of sp, cum, and cot-4mutants (at 25 C) (PB). Used to study development of crystalline inclusions (17). The cr sn double mutant grows as small, discrete, conidiating colonies suitable for velvet replication. The double mutant cr snresembles the rg cr double mutant phenotypically and has the advantage of fertility in homozygous crosses (796); for example of application, see reference 180.	IR	B
trp-2	VIR. Right of del (0 to 13%). Left of un-23 (5 to 27%), T(OY320), and ws-1 (38%) (818, 822, 1019, PB). Uses kynurenine, anthranilic acid, indole, or tryptophan (96). Kynurenine is utilized by conversion to anthranilate (447). Inferred to be the structural gene for the alpha subunit of the anthranilate synthetase complex (546). The gene product catalyzes anthranilate synthesis with ammonia but not with glutamine as the amino donor (29). Specifies anthranitate synthetase (glutamine linked) in collaboration with trp-1 in trifunctional trp-1+-trp-2+ enzyme aggregate (181, 259) (Fig. 11); see trp-1. Nonsense allele used to isolate supersuppressors (954) and to study enzyme complex restored by supersuppressors (183).	VIR	B
cyh-1	IR. Right of nit-1 (6%). Left of T(STL76) and al-2 (8 to 13%) (496, 797, 808).Resistant to cycloheximide (496, 748). Resistance is recessive in duplications (1090). Dominance reported in forced heterokaryons (496, 748) may have been due to skewed nuclear ratios (1090). Protein synthesis on ribosomes of the mutant cyh-1 proceeds in the presence of cycloheximide in a cell-free system (834). Readily scored on slants with 10 µg of cycloheximide per ml autoclaved in the medium. Excellent as a marker and valuable for selecting somatic recombinants or deletions in heterozygous duplications (748, 1091). Used to show that the cycloheximide-induced phase shift of the circadian clock involves protein synthesis (738). Called act-1: actidione resistant-1.	IR	B
cr-1	IR. Right of ace-7 (1 to 3%) and nic-2 (4 to 7%). Left of cys-9 (3%) and un-1(5%) (721, 816). Included in duplications from T(4540), which do not include cr-2 or cr-3(PB). (610) Rapid conidiation close to surface of agar. Produces very short conidiophores, bearing conidia in tight clusters (610, 611). Photographs (533, 634). Recessive. Deficient in adenylate cyclase (1066); has little or no endogenous adenosine 3',5'-phosphate (1065, 779). Abnormal morphology partially corrected by exogenous adenosine 3',5'-phosphate (891, 892, 1065, 1066). Guanosine 3',5'-phosphate also stimulates mycelial elongation (892). Cyclic nucteotide levels differ in mycelia and conidia (891, 892). NAD(P) glycohydrolase is overproduced and excreted; this is normalized by adenosine 3',5'-phosphate (533). Induction and localization of p-glucosidase is altered; induction is normalized by adenosine 3',5'-phosphate (906). Inability to use glycerol and certain other carbon sources is also overcome by adenosine 3',5'phosphate (598, 1067). Phosphodiesterase inhibitors do not counteract the morphological effect of cr-1 (892). Increased lactate dehydrogenase activity (92). Used to determine what functions are controlled by adenosine 3',5'-phosphate (779). Used to study adenosine 3',5'-phosphate binding protein (1082). Strains carrying the various alleles vary in growth habit (B123 strains are flat, restricted; allele L strains are spreading, but morphology may vary on different media). Modifier mutations which alter morphology and the ability of cr-1 to use glycerol occur frequently (383, 905). Crosses homozygous for allele B123 exude intact linear asci (634). Double mutants sn cr and cr rg form small conidiating colonies suitable for replica plating with velvet (182, 634, 796, 932, 1020). The triple mutant sn cr;csp-2 can be overlayered (744; photograph 747). The single mutant (B123) can be replicated by using a needle replicator (634). Scorability and viability are good. Excellent as a marker. Carotenoids formed normally. cr-1 ascospores may require longer to mature than cr+ ascospores. Allele CE4-11-67 called con(716, 717).	IR	B
ad-2	IIIR. Between thi-2 (1%) and trp-1 (1 to 7%) (11, 219). (482) Requires adenine or hypoxanthine (682). Controls conversion of phosphoribosylformylglycineamidine to AIR (120) (Fig. 8). Strains carrying allele 70004(t) are heat sensitive (34°C versus 25 C) (682) and osmotic remediable (636). Called complementation group H.	IIIR	B
uvs-2	IVR. Right of cys-4 (5%) (1023). Left of pmb (8%) (S. Ogilvie-Villa, cited in reference 248; R. Sadler and S. Ogilvie-Villa, personal communication) and the T(S4342) right breakpoint. Linked to T(AR209), T(T54M50), and T(ALS179) (2 to 6%), which mark the IVR tip (808). Sensitive to UV (273, 1023), ionizing radiation (537, 935, 940), methyl methane sulfonate (536, 537), nitrosoguanidine (509, 935), mitomycin C (537), 4-nitroquinoline 1-oxide (509), nitrous acid (D.R. Stadler and E. Crane, personal communication), and ICR-170 (509). Slight or no sensitivity to histidine (537, 759). No dimer excision (1164). Normal spontaneous mutation (275). High UV-induced mutation rate (273); for mutation induction by other agents, see references 509 and 940. Homozygous fertile; no effect on meiosis or crossing over. Recessive in heterokaryons (1023). uvs-2 is the most UV sensitive of Neurosporamutants (15 to 20 times wild type) (537, 938). Used to show that DNA repair is induced by a small dose of UV (1022). Used to demonstrate postreplication repair (130). Only known allele was discovered in several Seattle stocks of mixed ancestry, and thus may be present in lab stocks elsewhere (1023; D.R. Stadler, personal communication). Not to be confused with a cytoplasmically determined UV-sensitive mutation called uvs-2 in reference 187, but now called [uvs(cyt)].	IVR	B