FGSC #2054

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Reporting Genes: al-2;trp-3;tyr-1;pdx-1;inl;chol-2;thi-3 ars(101)

Species: crassa

Allele: 15300;td37;Y6994;37803;no#;47904(t);18558 101

Alternate Strain Number: 4-a all link

Depositor: RLM

Linkage Group: IR;IIR;IIIR;IVC;VR;VIL;VIIR R

Mating Type: a

Species Number: 10

Opposite Mating Type: 2053

Deposit Sheet ↗

Genes

Locus	Cultural Requirements	Link Group	Type
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
ars(101)	Grows on minimal, makes color reaction with p-nitrophenyl sulfate.	VII	B
tyr-1	IIIR. Right of vel (3 to 5%) and phe-2 (2 to 4%). Left of un-17 (4%) (316, 816, PB; R.L. Metzenberg, personal communication). (47). Requires tyrosine (1055). Lacks prephenate dehydrogenase activity (40, 316) (Fig. 11). Shows phenotypic adaptation after a lag, attaining the wild-type growth rate on minimal medium. Adaptation is not carried through conidia (1055). Allele UT145 formerly called tyr-3 (316).	IIIR	B
thi-3	VIIL. Between nic-3 (9 to 18%) and T(T54M50) (808, 812, 816). (482). Uses thiamine or thiazole (1059). Does not undergo growth adaptation on minimal medium. Growth on minimal medium is leaky at first, but becomes tight with exhaustion of endogenous thiazole (302), so scoring is best done late.	VIIL	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
chol-2	VIL. Left of nit-6 (6 to 8%) (812, PB). Requires choline (471). Also uses di- but not monomethylaminoethanol (468) (Fig. 12). Deficient in S-adenosylmethionine:phosphatidyl- monomethylethanolamine methyltransferase (222, 923, 924). Strains carrying the only allele, 47904t, are leaky on minimal medium at 22°C but not at 34°C (501). Phospholipid composition is abnormal on limiting choline (501). Growth is colonial on limiting supplement at 34°C and on minimal medium at 25°C.	VIL	B
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
trp-3	IIR. Right of fl (2 to 6%). Left of rip-1 (9%) and un-5(10%) (816, PB). (1166). Uses tryptophan (685); strains carrying some alleles also use indole (4). Structural gene for tryptophan synthetase (1167), called tryptophan desmolase in early literature. Tryptophan synthetase catalyzes three reactions: indoleglycerol-phosphate -> tryptophan, indole tryptophan, and indoleglycerol-phosphate <-> indole (Fig. 11). In Neurospora, all three reactions are catalyzed by a single protein, which is specified by a single gene (645, 1167). Mutants lack indoleglycerol-phosphate -> tryptophan activity but differ with respect to the other activities; e.g., strains carrying trp-3 allele (td141 are blocked in indoleglycerol-phosphate utilization but can use indole; trp-3 (td100) can synthesize indole but not convert it to tryptophan; trp-3 (td140) lacks all three activities. (See references 582 and 1049 for citations and characteristics of other mutants.) Used extensively for studies of gene structure in relation to enzymatic activity (257, 582 and references therein, 1167). The active enzyme is a homooligomer (645) thought to have two domains (644 and references therein). Biochemical studies of complementation between alleles: in vivo (582, 583) and in vitro (1048 and references therein). Complementation maps (4, 5, 9 and references therein, 582). Fine-structure maps (5, 540, 582, 1049). Reviewed as example of gene fusion (218). trp-3 mutant C83 provided the first proved example in Neurospora of gene-controlled loss of enzyme activity (685); trp-3 mutant S1952 provided the first example of allele-specific suppression restoring functional wild-type-like enzyme (1166). Allele td140 is supersuppressible (954, 955). Certain classes of trp-3mutants are osmotic remediable (583). Called td and tryp-3.	IIR	B