FGSC #7882

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Reporting Genes: sn cr-1;mtr uvs-2;lys-5 trp-2

Species: crassa

Alternate Strain Number: 7

Depositor: DRS

Linkage Group: IC R;IVR R;VIL R

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
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
mtr	IVR. Between pdx-1 (2%) and col-4 (1%) (101, 1017).Resistant to 4-methyltryptophan and p-fluorophenylalanine. pmn (= Pm-N, pm n), selected by resistance to p-fluorophenylalanine, has been shown to be alletic with mtr(R. Sadler and S. Ogilvie-Villa, personal communication; see also reference 248). Defective in transport of neutral aliphatic and aromatic amino acids via amino acid transport system I (as defined in reference 777) (248, 602, 1017, 1152). Causes an alteration in surface glycoproteins (1038). Used extensively for transport studies (247a, 1150 [review], 1152), also for studies of the mechanism of intralocus recombination (1021). Resistance is recessive in duplications from T(S1229) (PB). Recessive resistance used in a heterokaryon test system for mutation studies (1020). Suppressors obtained and used for selecting other resistance mutants (106, 107, 555, 1018). Allele 26 is a putative frameshift mutation reverted by ICR170 (106, 107). mtrascospores are slow to darken and mature; up to 50% of the young ascospores from heterozygous crosses are white (152, PB). With probable allele MN18, ascospore viability is improved by the addition of peptone to the crossing medium when the male parent is added (152). mtr has been scored on media containing 10 or 70 µg of filter-sterilized 4-methyltryptophan per ml or on 20 or 60 µg of p-fluorophenylalanine per ml (550, 1021, PB). Unlike 4-methyltryptophan, p-fluorophenylalanine is heat stable and can be added before autoclaving. Strains with mutations at the mtr locus may be obtained by selection for resistance to numerous agents or for defects in uptake ability. Thus, there is confusion in nomenclature. Genes originally designated neua, neur, neut, tru(628) may be mtr alleles. mtr was initially called mt (602).	IVR	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
lys-5	VIL. Right of cyt-2 (6%), aro-6 (3%), and cpl-1 (5 to 7%). Left of un-4 (2%) (1012, PB).Requires lysine. Partial response to glutaric acid (762). Lacks homocitrate synthase activity (464, 762) (Fig. 16). Some alleles such as 37402, called asco, are autonomous ascospore lethals or semilethals, resulting in mostly immature white spores (see reference 1012 for a photograph). Viability of the lys- spores is improved by long incubation (7). With other alleles such as DS6-85, ascospores blacken and germinate normally. Accumulates malate plus citrate on media with limiting lysine concentrations (464). Four complementation groups (12). Allele 37402 called asco.	VIL	B