FGSC #5203

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Mutant Type

Genus: N

reporting_genes: un-5;cys-10 uvs-2;al-3 inl his-6

species: Neurospora crassa

allele: b39t 39816 no# RP100 83201t Y152M105

stock: M2164

glasgow:

mutagen:

Depositor: EK

Link Group: IL;IVL IVR;VR VR VR

MT: a

Species No: 10

gene_back:

oppmt: 5202

trans:

ref1:

ref2:

site:

country:

ksudc_link: https://digital.lib.k-state.edu/item/neurospora-crassa/fgsc-5203

ksudc_link_html: https://digital.lib.k-state.edu/item/neurospora-crassa/fgsc-5203 ↗

Genes

Locus	Cultural Requirements	Link Group	Type
uvs-2	IVR. Right of cys-4 (5%) (1023). Left of pmb (8%) (S. Ogilvie-Villa, cited in reference 248; R. Sadler and S. Ogilvie-Villa, personal communication) and the T(S4342) right breakpoint. Linked to T(AR209), T(T54M50), and T(ALS179) (2 to 6%), which mark the IVR tip (808). Sensitive to UV (273, 1023), ionizing radiation (537, 935, 940), methyl methane sulfonate (536, 537), nitrosoguanidine (509, 935), mitomycin C (537), 4-nitroquinoline 1-oxide (509), nitrous acid (D.R. Stadler and E. Crane, personal communication), and ICR-170 (509). Slight or no sensitivity to histidine (537, 759). No dimer excision (1164). Normal spontaneous mutation (275). High UV-induced mutation rate (273); for mutation induction by other agents, see references 509 and 940. Homozygous fertile; no effect on meiosis or crossing over. Recessive in heterokaryons (1023). uvs-2 is the most UV sensitive of Neurosporamutants (15 to 20 times wild type) (537, 938). Used to show that DNA repair is induced by a small dose of UV (1022). Used to demonstrate postreplication repair (130). Only known allele was discovered in several Seattle stocks of mixed ancestry, and thus may be present in lab stocks elsewhere (1023; D.R. Stadler, personal communication). Not to be confused with a cytoplasmically determined UV-sensitive mutation called uvs-2 in reference 187, but now called [uvs(cyt)].	IVR	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
cys-10	IVL. Left of acon-3 (1 to 6%), ace-4 (19 to 33%), and cut (28 to 37%) (578, PB). (721) Uses cysteine, cystathionine, homocysteine, or methionine, with a slight response to thiosulfate (469, 596, 721); however, E. Kafer (personal communication) found good growth on thiosulfate. Growth is better on casein hydrolysate than on methionine (D.D. Perkins, unpublished data). cys-10 chol-1double mutants grow better on methionine alone than on methionine plus choline (721). Lacks sulfite reductase, as do cys-2 and cys-4mutants (596). Formerly called met-4; see reference 721.	IVL	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
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
un-5	IL. Right of fr (6%). Left of T(39311) and nit-2 (2%) (816, 798). (574). Unknown function. Heat sensitive, 34°C versus 23°C. Inhibited by histidine and tryptophan: osmophilic (26 to 28 C) (574, 575). Formerly called un(b39).	IL	B