FGSC #4553

Mutant Type

Genus: N

reporting_genes: cyh-1 al-2 al-1;al-3

species: Neurospora crassa

allele: KH52(r) 15300 34508;RP100

stock: 9325

glasgow:

mutagen:

Depositor: DDP

Link Group: IR IR IR;VR

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-4553

ksudc_link_html: https://digital.lib.k-state.edu/item/neurospora-crassa/fgsc-4553 ↗

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 (797, 808; D.D. Perkins, unpublished data).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
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
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
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