FGSC #4554

Mutant Type

Genus: N

reporting_genes: cyh-1 al-2 al-1;al-3 inl;bd;csp-2

species: Neurospora crassa

allele: Kh52(r) 15300 34508;RP100 83201(t);no#;UCLA101

stock: 9328

glasgow:

mutagen:

Depositor: DDP

Link Group: IR IR IR;VR VR;IVR;VIIL

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-4554

ksudc_link_html: https://digital.lib.k-state.edu/item/neurospora-crassa/fgsc-4554 ↗

Genes

Locus	Cultural Requirements	Link Group	Type
bd	Because dense bands of conidia are produced on appropriate solid medium at intervals of about 24 hr (1792, 1794), the mutant has been used extensively to study circadian rhythms (239, 560, 621, 1382, 1794). bd has no effect on the underlying clock mechanism, but allows the visible expression of rhythm (622). Grow rate is about 70% that of the wild type (232). Conidiation is enhanced, even on slants (232). CO2 inhibits conidiation and, thus, inhibits banding; bd is much less sensitive than wild type to this effect of CO2 (1792). Biotin starvation leads to a phenocopy in wild type and to increased persistence of banding in bd (2206). Originally identified in a bd; inv strain called "timex" (1791). bd alone is sufficient to cause banding (1794). Used to study conidiation under nonstarvation conditions (1820). Used in a study of morphological differentiation patterns such as concentric rings and radial zonations (528). Expression is affected by changing the concentrations of agar, sugar, and salts. Conidial scatter is eliminated in the double mutant bd; csp (239). Conveniently scored by conidial banding on agar in long tubes or large plates at 25oC in constant dark or in a dark-light cycle, but not in constant light (1791).	IVR	B
inl	VR. Between pho-3 (3 to 4%) and pab-1 (1 to 10%). Right of al-3 (362, 397, 1036). (482)Requires inositol (65). Lacks D-myoinositol-1-phosphatase (1142). Lack of glucocycloaldolase found by Pina and Tatum (826) is attributed by Williams (1142) to drastic repression of glucocycloaldolase by the concentration of inositol used for growth. Growth is colonial on low levels of inositol (367). Tends to extrude dark pigment into the medium when grown on suboptimal inositol. Composition of phospholipids and cell walls is abnormal on limiting inositol (367, 439, 440, 501). Inhibited by hexachlorocyclohexane (366, 457, 931). Conidia are subject to death by unbalanced growth on minimal medium (1028, 1033), a property exploited for mutant enrichment ("inositol-less death") (606, 647) because double mutants are at a selective advantage. Heat-sensitive allele 83201 is especially useful for mutant enrichment (832, 1043). Used in the first experiments reporting transformation of Neurospora by N. crassaDNA (677, 679) and reported to be efficient as a recipient in absence of inositol (1162). Used to study glucose (917) and sulfate (641) transport systems. Used extensively for studying induced reversion (392). Used for studying the mechanism of inositol-less death (647, 702), mutagenicity of ferrous ions, and regulation of mitochondrial membrane fluidity; for a review, see reference 702. Spontaneous reversion rates (386). Allele-specific partial suppressor (390). Allele 46802 is nonrevertable and inseparable from translocation 46802 (386, 808). Strains carrying heat-sensitive allele 83201 show slow semicolonial growth in liquid minimal medium at 25°C (641), but look normal on slants (D.D. Perkins, unpublished data). Strains carrying allele 89601 contain cross-reacting material (1183). Mutant gene exo-1 is present in the inl(89601) a stock FGSC 498 and may, therefore, be present in stocks of mutants derived by inositol-less death. (See references 194, 325, and 1027). Called inos.	VR	B
csp-2	VIIL. Linked to thi-3 (<1%), probably to the right. Left of T(T54M40) (972, PB). Conidia fail to separate and become airborne. Cultures on agar readily scored by the tap test. Resembles csp-1. Conidia are freed in water suspension long after induction of aerial growth and at only 1/100 the concentration of the wild type. A csp-1;csp-2double mutant releases no detectable free conidia under the same conditions (972). Most csp-2alleles complement csp-1 in forced heterokaryons to form the wild-type number of free conidia (972), but csp-2(UCLA102) does not (969). Conidiating colonies of the csp-2;sn cr-1 strain on replica plates can be overlayered without the conidia being spread (744); photograph (747).	VIIL	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
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-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
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