FGSC #5188

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Reporting Genes: sn cr-1;acr-2;cys-10 pdx-1 pan-1 uvs-2

Species: crassa

Allele: C136 B123 KH5(r) 39816 37803 5531 no#

Alternate Strain Number: M1989

Depositor: EK

Linkage Group: I IR;III;IVL IVR IVR IVR

Mating Type: a

Species Number: 10

Deposit Sheet ↗

Genes

Locus	Cultural Requirements	Link Group	Type
acr-2	III. Linked to thi-4 (0/286). Left of sc (3 to 6%) and spg (1 to 11%) (498, 816). acr-2 has been shown left of the centromere on published maps but without direct evidence. acr-2and trp-1 (on IIIR) cosegregated at the second division in 1 of 13 asci (H.B. Howe, Jr., personal communication), which would favor a right arm location. Resistant to acriflavine (494, 495); also resistant to 3-amino-1,2,4-triazole (seven alleles tested) (494). Resistance is probably dominant (heterokaryon tests) (498). Not resistant to malachite green. An excellent stable marker, fully fertile, with unambiguous scoring. Sizable inocula should be used to avoid false-negative tests. Use acriflavine at 50 µg /ml in minimal agar medium (816) (higher concentrations may be used) and aminotriazole at 0.5 mg/ml; both added before autoclaving.	III	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
cys-10	IVL. Left of acon-3 (1 to 6%), ace-4 (19 to 33%), and cut (28 to 37%) (578, PB). (721) Uses cysteine, cystathionine, homocysteine, or methionine, with a slight response to thiosulfate (469, 596, 721); however, E. Kafer (personal communication) found good growth on thiosulfate. Growth is better on casein hydrolysate than on methionine (D.D. Perkins, unpublished data). cys-10 chol-1double mutants grow better on methionine alone than on methionine plus choline (721). Lacks sulfite reductase, as do cys-2 and cys-4mutants (596). Formerly called met-4; see reference 721.	IVL	B
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
pdx-1	IVR. Right of pyr-1 (<1 to 10%). Left of T(S1229) and pt (2%) (40, 55, 692, 808). (482) Uses pyridoxine, pyridoxal, or pyridoxamine (843, 845, 846). Shows intralocus complementation (845, 846) and recombination (848), Provided the first proven example of gene conversion (686). Scoring is sharpened by addition of 100 mg of desoxypyridoxine per liter (845). Several alleles (called pdxp: e.g., 44602) are pH sensitive and can grow without pyridoxine on medium containing ammonium ions at a pH above 6 (1029). Conidia are subject to death by unbalanced growth on minimal medium (1033). A yellow pigment is excreted under certain conditions by the pdx-1;En(pdx) double mutant; see En(pdx). Allele 44204 originally called pdx-2 (see reference 848).	IVR	B
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
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