FGSC #8935

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Reporting Genes: al-2; inl; poi-2 arg-10 nt

Species: crassa

Allele: poi-2(1)

Depositor: MAN

Linkage Group: VII

Mating Type: a

Species Number: 10

Deposit Sheet ↗

Genes

Locus	Cultural Requirements	Link Group	Type
poi-2	VIIR. Linked to cat-2 (0 or 1T/18 asci), cox-8 (1T/18 asci). The second most abundant cDNA isolated from starved mycelial and perithecial tissues. A novel sequence.	VIIR	B
nt	VIIR. Between arg-10 (2 to 12%) and sk (7 to 18%) (789). (874) Uses nicotinic acid. May respond also to tryptophan, phenylalanine, tyrosine, quinic acid, and precursors of nicotinic acid or tryptophan, or both, depending on genetic background (448, 760). Best supplemented with nicotinamide and scored as a nic mutant. Probably deficient in tryptophan pyrrolase (tryptophan 2,3-dioxygenase) (Fig. 18), but direct evidence is lacking because tryptophan oxygenase cannot be assayed in Neurospora (368). Kynurenine formamidase levels are normal (368). Pyridine nucleotide levels (111).	VIIR	B
arg-10	Uses arginine but not precursors.	VIIR	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
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