FGSC #5219

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Reporting Genes: un-5 leu-3 cr-1 cyh-1 al-2 nic-1

Species: crassa

Allele: b39t R156 B123 KH52(r) 15300 S1413

Alternate Strain Number: M1611

Depositor: EK

Linkage Group: IL IL IR IR IR IR

Mating Type: A

Species Number: 10

Deposit Sheet ↗

Genes

Locus	Cultural Requirements	Link Group	Type
un-5	IL. Right of fr (6%). Left of T(39311) and nit-2 (2%) (816, 798). (574). Unknown function. Heat sensitive, 34°C versus 23°C. Inhibited by histidine and tryptophan: osmophilic (26 to 28 C) (574, 575). Formerly called un(b39).	IL	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
cr-1	IR. Right of ace-7 (1 to 3%) and nic-2 (4 to 7%). Left of cys-9 (3%) and un-1(5%) (721, 816). Included in duplications from T(4540), which do not include cr-2 or cr-3(PB). (610) Rapid conidiation close to surface of agar. Produces very short conidiophores, bearing conidia in tight clusters (610, 611). Photographs (533, 634). Recessive. Deficient in adenylate cyclase (1066); has little or no endogenous adenosine 3',5'-phosphate (1065, 779). Abnormal morphology partially corrected by exogenous adenosine 3',5'-phosphate (891, 892, 1065, 1066). Guanosine 3',5'-phosphate also stimulates mycelial elongation (892). Cyclic nucteotide levels differ in mycelia and conidia (891, 892). NAD(P) glycohydrolase is overproduced and excreted; this is normalized by adenosine 3',5'-phosphate (533). Induction and localization of p-glucosidase is altered; induction is normalized by adenosine 3',5'-phosphate (906). Inability to use glycerol and certain other carbon sources is also overcome by adenosine 3',5'phosphate (598, 1067). Phosphodiesterase inhibitors do not counteract the morphological effect of cr-1 (892). Increased lactate dehydrogenase activity (92). Used to determine what functions are controlled by adenosine 3',5'-phosphate (779). Used to study adenosine 3',5'-phosphate binding protein (1082). Strains carrying the various alleles vary in growth habit (B123 strains are flat, restricted; allele L strains are spreading, but morphology may vary on different media). Modifier mutations which alter morphology and the ability of cr-1 to use glycerol occur frequently (383, 905). Crosses homozygous for allele B123 exude intact linear asci (634). Double mutants sn cr and cr rg form small conidiating colonies suitable for replica plating with velvet (182, 634, 796, 932, 1020). The triple mutant sn cr;csp-2 can be overlayered (744; photograph 747). The single mutant (B123) can be replicated by using a needle replicator (634). Scorability and viability are good. Excellent as a marker. Carotenoids formed normally. cr-1 ascospores may require longer to mature than cr+ ascospores. Allele CE4-11-67 called con(716, 717).	IR	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
leu-3	IL. Right of the In(OY323) left breakpoint and nit-2 (12 to 18%). Left of cyt-1 (5 to 8%) and T(OY321) (57, 816, PB; D.D. Perkins, N.B. Raju, and E.G. Barry, in preparation). (868)Requires leucine (867, 868). Regulatory mutation; prevents synthesis of alpha-isopropylmalate isomerase and beta-isopropylmalate dehydrogenase and prevents full derepression of alpha-isopropylmalate synthetase; also involved in regulation of isoleucine and valine synthesis, q.v. (427, 771, 833) (Fig. 15). The original allele, 47313, is leaky, but some other alleles, e.g., R156, are not.	IL	B
nic-1	IR. Right of ace-3 (<1%), lys-1 (1%), and In(OY323). Left of os-1(10 to 29%) (2, 57, 131, 578, 789, 816, 907). (482) Uses nicotinic acid or nicotinamide, but not precursors (97, 100) (Fig. 18). Accumulates quinolinic acid (100). Used to study intralocus recombination (907). Called the q locus.	IR	B