FGSC #288

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Reporting Genes: cr-1 nit-1 al-1 os-1

Species: crassa

Allele: B122 34547 34508 B135

Alternate Strain Number: 1124

Depositor: DDP

Linkage Group: IR IR IR IR

Mating Type: a

Species Number: 10

Opposite Mating Type: 258

Deposit Sheet ↗

Genes

Locus	Cultural Requirements	Link Group	Type
nit-1	IR. Right of Tp(T54M94) and ad-9 (3 to 15%). Left of cyh-1(6%) (466, 496, 816). (482)Cannot use nitrate or hypoxanthine as a nitrogen source, but uses nitrite, ammonia, or amino acids (1000). Does not prevent formation or nitrate reductase apoprotein (999), but lacks the molybdenum-containing cofactor common to nitrate reductase and xanthine dehydrogenase (591, 741) (Fig. 19 and 24). The nitrate reductase in nit-1 extracts does not catalyze the complete electron transport sequence from NADPH to N03 but does catalyze the initial part of this sequence if a suitable electron acceptor (e.g., cytochrome c) is provided (999). See reference 198 for a model of interaction of nit-1 and nit-3 gene products. See references 226, 999, and 1000 for regulation.	IR	B
os-1	IR. Between nic-1 (10 to 29%) and arg-13 (1%) (789, 812, 816). (M.R. Emerson, cited in reference 789) Sensitive to high osmotic pressure. Readily scored by morphology on nonmoist slants or by failure to grow on media with 4% NaCl. Most os-1 alleles result in cultures that form no or few conidia on agar slants. Alleles NM233t and NM204t are heat sensitive (25°C versus 34°C). In media of high osmolarity, os-1 strains form protoplasts (323, 438). os-1 (Bl35) is an essential genotypic component of the wall-less strain slime (321). Protoplasts of strains carrying heatsensitive allele NM233t are stable at 37 C, with a 7.5-h redoubling time, and show good regeneration. The biochemical defect differs from that affected by either polyoxin or sorbose (chitin or glucan syntheses) (970, 971). Cell wall pores are four times larger in an os-1 mutant than in the wild type; os-1 also has a higher exclusion threshold and a 30-fold-higher galactosamine/ glucosamine ratio (1083, 1084). Intralocus complementation (676). Allele Y256M209 called flm-1.	IR	B
al-1	IR. Right of hom (<1%), arg-6 (<1 to 4%), T(T54M94), and al-2. Left of lys-3 (9%). (797, 808; D.D. Perkins, unpublished data). (482) Carotenoids abnormal. Strains carrying the various alleles differ widely in phenotype, ranging from white (e.g., 4637) and "aurescent" (pigment in peripheral conidia and conidiophores, 34508) to yellow mycelia and conidia (e.g., ALS4 and RES-25). See, for example, reference 1042. Strains carrying alleles ALS-14, RES-6, 34508, and RES-25 contain large amounts of phytoene (99 to 100% of the total neutral carotenoids), suggesting a lesion that affects phytoene dehydrogenase (398, 1039) (see Fig. 9). Strains carrying allele RWT-ylo accumulate zeta carotene and smaller amounts of neurosporene, suggesting a leaky block of the step between these intermediates (1071). It is not known whether phytoene dehydrogenase catalyzes the whole series of dehydrogenations or whether leakiness of this enzyme accounts for the different mutant phenotypes. For complementation tests, see references 500, 1039, and 1041. Fine-structure mapping (500, 1042). Translocation T(4637), inseparable from al-1, was the first albino mutation and one of the first chromosome rearrangements in Neurospora to be identified and studied (656). Allele 34508 called aur: aurescent.	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