FGSC #237

Mutant Type

Genus: N

reporting_genes: fr cr-1 al-1

species: Neurospora crassa

allele: B110 L 34508

stock: 1107

glasgow:

mutagen:

Depositor: DDP

Link Group: IL IR IR

MT: A

Species No: 10

gene_back:

oppmt: 0

trans:

ref1:

ref2:

site:

country:

ksudc_link: https://digital.lib.k-state.edu/item/neurospora-crassa/fgsc-237

ksudc_link_html: https://digital.lib.k-state.edu/item/neurospora-crassa/fgsc-237 ↗

Genes

Locus	Cultural Requirements	Link Group	Type
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 (797, 808; D.D. Perkins, unpublished data).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
fr	IL. Between ro-10 (18%) and un-5 (6%) (798, PB). (789)Delicate branching on agar surface and delicate aerial growth with no conidia (789). Multiple hyphal branching (382). Deficient in glucose- 6-phosphate dehydrogenase (as are col-2 and balmutants) (949, 952). Partially deficient in linolenic acid (115); morphology partially corrected by exogenous linolenic acid (892, 943). Low adenylate cyclase activity and low adenosine 3',5'-phosphate (943, 950). Used to determine what functions are controlled by adenosine 3',5'-phosphate (779). Unlike cr-1, fr is not corrected morphologically by exogenous cyclic nucleotides (892, 951). Scott (943) reported that morphology is corrected by theophylline; Rosenberg and Pall (892) reported no correction by phosphodiesterase inhibitors. Cell wall analysis; photograph (112, 278, 946). Reduced amount of cell wall peptides (1165). Recessive in duplications (808). Female sterile. Both known alleles (B110 and R2499) revert to fr+.	IL	B