FGSC #1284

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Reporting Genes: T(V;VI)46802 inl his-1 pk chol-2 ad-8

Species: crassa

Allele: 46802 C84 B6;47904 Y226M58

Alternate Strain Number: 5-6-181

Depositor: DDP

Linkage Group: VR;VIL

Mating Type: a

Species Number: 10

Opposite Mating Type: 1283

Deposit Sheet ↗

Genes

Locus	Cultural Requirements	Link Group	Type
pk	bis, biscuit) VR. Between met-3 (1%) and T(EB4)^L, cot-2 (8%), cl (2%). Growth on an agar surface is initially colonial and flat. A mass of aerial hyphae is then sent up, which conidiates profusely (1548). Somewhat similar in morphology to sn, cum, sp, and cot-4 at 25ºC, but distinguishable. Hyphae branch dichotomously (1405, 1548). Increased activity of L-glutamine:D-fructose-6-phosphate amidotransferase was observed in crude extracts of one pk strain, but not in nine others; increased activity for this enzyme also was found in cl and in four other nonallelic morphological mutants (1758). Hexoseaminoglycan consists of a single component on medium without sorbose, in contrast to two components in wild type (1960). Antigenic surface mucopolyoside (532). Cell-wall analysis and photograph, allele B6 (507) and allele C-1810-1 (287). Cell-wall enzymes (633). Effect of carbon source (531). One observation suggested a functional interaction with cl (1965), but substantial crossing-over frequencies and recovery of the double mutant pk cl indicated that the loci are distinct (569). The gene was named for the vegetative mutant phenotype, which is recessive. Several alleles were called bis (1592). The sexual phase is also affected. Asci are thin-walled, bulbous, and nonlinear in homozygous pk ´ pk crosses (1406, 1409, 1550). Spindle orientation is abnormal in the swollen asci, and no apical pore is formed (1625, 1679). Most mutant alleles are recessive for the ascus effect, but some are dominant with variable penetrance. Sorbose-resistant mutants at various loci act as dominance modifiers of the ascus effect of dominant alleles (1757). Sexual-phase-recessive allele C-1610 and dominant allele 17-088 are both associated with reciprocal translocations (1578).		B
T(V;VI)46802	Translocation		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
his-1	VR. Right of ure-1 (1%). Left of pho-2 (3%), al-3, and inl (1 to 10%) (397, 570, 578, 1036). (434)Requires histidine (434). Accumulates imidazole glycerol phosphate. Lacks imidazole glycerol phosphate dehydrase (24, 25) (Fig. 14). Intralocus complementation (162). Recombination between his-1 alleles is controlled by rec-1(172, 520, 1070). Initial his-1 allele called C84.	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
ad-8	VIL. Right of ser-6 (15%) and het-8 (12%). Left of aro-6 (8%) and cpl-1(6 to 11%) (437, 510, 730, PB). Requires adenine; cannot use hypoxanthine (526). Lacks adenylosuccinate synthase (511) (Fig. 8). Fine-structure mapping and intralocus complementation (510-512). Has little hypoxanthine uptake and little hypoxanthine phosphoribosyltransferase; both these effects are partly counteracted in ad-1 ad-8 double mutants (903). Little hypoxanthine phosphoribosyltransferase is also found in mep(3) and mep(10)mutants, q.v. Used to study purine transport (787, 903, and references therein). Called complementation group E.	VIL	B