FGSC #8374

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Reporting Genes: his-3 cyh-1; Bml[r]; inl a[m33]

Species: crassa

Allele: 1-234-723, KH52(r), 511(r); 37401

Alternate Strain Number: RLM32-29

Depositor: RLM

Linkage Group: I,V,VI

Mating Type: a

Species Number: 10

Genetic Background: OR

Deposit Sheet ↗

Genes

Locus	Cultural Requirements	Link Group	Type
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
a[m33]			B
Bml[r]			B
his-3	IR. Right of met-10 (R.L. Metzenberg, personal communication). Left of cog (1 to 3%) (172,174), ure-4 (1%) (78), and ad-3A (1%) (271). (434)Requires histidine (434). Complex gene coding for histidinol dehydrogenase, phosphoribosyladenosine 5'-triphosphate-pyrophosphohydrolase, and phosphoribosyl-adenosine 5'-monophosphate-cyclohydrolase (16, 673) (Fig. 14). All three activities appear to be catalyzed by a single protein (673). Strains carrying different individual alleles may lack only the early reaction(s) or only histidinol dehydrogenase, or both. Those that lack only histidinol dehydrogenase accumulate histidinol (16, 162, 1123). Mutants produce cross-reacting material (220). Used to study intralocus complementation and recombination (15, 16, 27, 162, 164, 171, 172, 1121, 1122, 1124). Intralocus recombination is regulated by cog and by rec-2 (27, 171); it is not affected by rec-1 (172). Translocation T(IR;VII)TM429, with one breakpoint in his-3, has been used to show that cog is cis-acting (171). Initial alleles: C140 and T1710 (= C1710).	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