FGSC #7266

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Reporting Genes: helper + ad-1;am132 inl inv mei-2

Species: crassa

Depositor: RLM

Mating Type: A

Species Number: 10

Deposit Sheet ↗

Genes

Locus	Cultural Requirements	Link Group	Type
am1			B
mei-2	VR. Linked near inl (995). Between al-3 (20 and his-6(A.L. Schroeder, personal communication). Meiotic divisions occur, and many ascospor are produced, but many are inviable and white. Crosses heterozygous or homozygous for Mei-2 give extensive nondisjunction of all linkage groups (995). Chromosome pairing much reduced (B.C. Lu, cited in reference 995). Sensitive to methyl methane sulfonate, histidine, and gamma rays (939). Dominant in the original strain (995), but progeny show incomplete penetrance (939).	VR	B
inv	VR. Right of pab-2 (3%) and ro-4 (5 to 8%), Left of asn (4 to 9%) (918, PB).Unable to use sucrose as a carbon source. Grows well on glucose or fructose and fairly well on Casamino Acids or yeast extract. Invertase structural gene; invertase deficient and uninducible by normal inducers. Makes cross-reacting material (919). Invertase is also affected by cot-2, q.v.	VR	B
inl	VR. Between pho-3 (3 to 4%) and pab-1 (1 to 10%). Right of al-3 (362, 397, 1036). (482)Requires inositol (65). Lacks D-myoinositol-1-phosphatase (1142). Lack of glucocycloaldolase found by Pina and Tatum (826) is attributed by Williams (1142) to drastic repression of glucocycloaldolase by the concentration of inositol used for growth. Growth is colonial on low levels of inositol (367). Tends to extrude dark pigment into the medium when grown on suboptimal inositol. Composition of phospholipids and cell walls is abnormal on limiting inositol (367, 439, 440, 501). Inhibited by hexachlorocyclohexane (366, 457, 931). Conidia are subject to death by unbalanced growth on minimal medium (1028, 1033), a property exploited for mutant enrichment ("inositol-less death") (606, 647) because double mutants are at a selective advantage. Heat-sensitive allele 83201 is especially useful for mutant enrichment (832, 1043). Used in the first experiments reporting transformation of Neurospora by N. crassaDNA (677, 679) and reported to be efficient as a recipient in absence of inositol (1162). Used to study glucose (917) and sulfate (641) transport systems. Used extensively for studying induced reversion (392). Used for studying the mechanism of inositol-less death (647, 702), mutagenicity of ferrous ions, and regulation of mitochondrial membrane fluidity; for a review, see reference 702. Spontaneous reversion rates (386). Allele-specific partial suppressor (390). Allele 46802 is nonrevertable and inseparable from translocation 46802 (386, 808). Strains carrying heat-sensitive allele 83201 show slow semicolonial growth in liquid minimal medium at 25°C (641), but look normal on slants (D.D. Perkins, unpublished data). Strains carrying allele 89601 contain cross-reacting material (1183). Mutant gene exo-1 is present in the inl(89601) a stock FGSC 498 and may, therefore, be present in stocks of mutants derived by inositol-less death. (See references 194, 325, and 1027). Called inos.	VR	B
am132			B
ad-3B	IR. Between ad-3A (0.1 to 0.7%) and nic-2 (3%) (271). (482) Uses adenine or hypoxanthine (682). Blocked in interconversion of AIR to CAIR (348) (Fig. 8). Produces purple pigment, permitting direct visual selection (276, 682). Pigment is secreted with low concentrations of adenine (e.g., 0.1 mM), not with high concentrations (2 mM) (276, 682, 785). Pigment production used to assess effect of histidine and tryptophan on purine nucleotide synthesis (786). Reduced interallelic fertility (264, 407). Complementation maps (268, 274). Relation of mutagens to complementation patterns (269). Mutants with non-polarized complementation patterns on the right side of the complementation map grow on minimal medium if supplied with CO2; other mutants do not respond to CO2, (270). Used extensively for mutagenesis (see ad-3A). Rearrangement T(I- >III)Y112M4i ad-3B, which has a breakpoint inseparable from ad-3B, was the first insertional translocation to be reported for fungi (266). Allele 7-017-0137 shows "fixed instability," mutating to an unstable prototrophic allele (41). Alleles 2-17-126, 12-21-28, and numerous others are supersuppressible (408, 749, 955). Called complementation group B.	IR	B
ad-1	VIL. Right of ylo-1 (6%). Left of the centromere (< 1 to 2%), T(AR209), and rib-1(3 to 5%) (1102, 1012). (482) Uses adenine or hypoxanthine (682, 824). Accumulates AICAR (81, 904) and SAICAR (81). May affect inosine 5'-monophosphate cyclohydrolase (902, 904) (Fig. 8). Used to study purine transport (903 and references therein). Ascospores are white in homozygous ad-1 x ad-1 crosses, and ad-1 ascospores may be white in heterozygous crosses (D.D. Perkins, unpublished data). Called complementation group M.	VIL	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