FGSC #7588

Mutant Type

Genus: N

reporting_genes: (dgr-1 at al-3 his-6 + a[m1] ad-3B cyh-1)

species: Neurospora crassa

allele: KHY15 M111 Rp100 Y152M105 + helper

stock: 5385

glasgow:

mutagen:

Depositor: DDP

Link Group: VL VC VR VR

MT: A

Species No: 10

gene_back: SL

oppmt: 7562

trans:

ref1:

ref2:

site:

country:

ksudc_link: https://digital.lib.k-state.edu/item/neurospora-crassa/fgsc-7588

ksudc_link_html: https://digital.lib.k-state.edu/item/neurospora-crassa/fgsc-7588 ↗

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
dgr-1	VL. Between rDNA, T(UK2-33), In(UK2-y)^L and T(AR30), caf-1 (7%). Resistant to 1 mM deoxyglucose, also resistant to sorbose at 5 mM. Grows more slowly that wild type on standard medium but growth is initially faster than that of wild type on media with mono- or disaccharides plus deoxyglucose. Conidiation is precocious.	VL	B
at	Grows on minimal media. Conidia form in clumps, especially at the top of a slant.	V	B
al-3	VR. Between his-1 and inl (1%) (1119, PB). Carotenoids deficient (398). Reported to lack geranylgeranyl pyrophosphate synthetase activity and is blocked in soluble fraction, consistent with lesion between isopentenyl pyrophosphate and geranylgeranyl pyrophosphate (445), but can still produce farnesyl pyrophosphate (445) and steroids (398). (See Fig. 9.) This evidence contradicts in vivo labeling results that indicate a lesion between prephytoene pyrophosphate and phytoene (572). Strains carrying allele Y234M470 (al-3ros), formerly called rosy (49), become partially pigmented but are readily distinguished from the wild type. ylo-1 can be scored in combination with al-3ros (Y234M470) (PB). Strains carrying other alleles (e.g., RP100) (1119) are white with a trace of pink pigment. Biosynthetic pathway for carotenoids. It is thought that the same prenyl transferase catalyzes all the steps from dimethylallyl pyrophosphate to geranylgeranyl pyrophosphate (444; R.W. Harding, personal communication), and it has been proposed that a separate prenyl transferase converts dimethylallyl pyrophosphate to farnesyl pyrophosphate for sterol synthesis (445). The conversion of phytoene to the various carotenoid pigments involves a series of dehydrogenations, cyclizations, and other reactions. There must also be a cis/trans isomerization analogous to that found in tomato (842). The sequence of some of these steps is still uncertain; the pathway must branch, and there may be alternate routes to some of the products. See references 228, 443, 444, 842 and citations therein for proposed sequences. al-1 is probably blocked in phytoene dehydrogenase (398). It is not known whether this enzyme catalyzes the whole series of dehydrogenations. al-2 is reported blocked between geranylgeranyl pyrophosphate and phytoene (445) and between prephytoene pyrophosphate and phytoene (572). al-3 is alternately reported blocked between isopentenyl pyrophosphate and geranylgeranyl pyrophosphate (445) and between prephytoene pyrophosphate and phytoene (572), but it is not blocked in the production of farnesyl pyrophosphate or sterols (398, 445). ylo-1 is evidently blocked in a late step, probably either in the conversion of lycopene to 3,4-dehydrolycopene or in the conversion of either torulene or gamma-carotene to neurosporaxanthin (see citations in reference 398).	VR	B
ad-3B	IR. Between ad-3A (0.1 to 0.7%) and nic-2 (3%) (271). (482) Uses adenine or hypoxanthine (682). Blocked in interconversion of AIR to CAIR (348) (Fig. 8). Produces purple pigment, permitting direct visual selection (276, 682). Pigment is secreted with low concentrations of adenine (e.g., 0.1 mM), not with high concentrations (2 mM) (276, 682, 785). Pigment production used to assess effect of histidine and tryptophan on purine nucleotide synthesis (786). Reduced interallelic fertility (264, 407). Complementation maps (268, 274). Relation of mutagens to complementation patterns (269). Mutants with non-polarized complementation patterns on the right side of the complementation map grow on minimal medium if supplied with CO2; other mutants do not respond to CO2, (270). Used extensively for mutagenesis (see ad-3A). Rearrangement T(I- >III)Y112M4i ad-3B, which has a breakpoint inseparable from ad-3B, was the first insertional translocation to be reported for fungi (266). Allele 7-017-0137 shows "fixed instability," mutating to an unstable prototrophic allele (41). Alleles 2-17-126, 12-21-28, and numerous others are supersuppressible (408, 749, 955). Called complementation group B.	IR	B
am1			B
his-6	VR. Right of un-9 (6%) and pyr-6 (6 to 18%). No recombination with terminal translocation T(NMI49) (793, 808, 816, 818, PB). Report of IV linkage (646) not confirmed.Requires histidine. Blocked before imidazole glycerol phosphate (162, 1123) (Fig. 14). No intralocus complementation (95 alleles) (162). Intralocus recombination (172).	VR	B