FGSC #7508

Mutant Type

Genus: N

reporting_genes: his-3 cyh-1 al-1;mtr;inl

species: Neurospora crassa

allele: 1-234-723 KH52(r) 34508;SR62;89601

stock: RLM77-06

glasgow:

mutagen:

Depositor: RLM

Link Group: IR R R;IVR;VR

MT: a

Species No: 10

gene_back: SL

oppmt: 7507

trans:

ref1:

ref2:

site:

country:

ksudc_link: https://digital.lib.k-state.edu/item/neurospora-crassa/fgsc-7508

ksudc_link_html: https://digital.lib.k-state.edu/item/neurospora-crassa/fgsc-7508 ↗

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 (797, 808; D.D. Perkins, unpublished data).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
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
his-3	IR. Right of met-10 (R.L. Metzenberg, personal communication). Left of cog (1 to 3%) (172,174), ure-4 (1%) (78), and ad-3A (1%) (271). (434)Requires histidine (434). Complex gene coding for histidinol dehydrogenase, phosphoribosyladenosine 5'-triphosphate-pyrophosphohydrolase, and phosphoribosyl-adenosine 5'-monophosphate-cyclohydrolase (16, 673) (Fig. 14). All three activities appear to be catalyzed by a single protein (673). Strains carrying different individual alleles may lack only the early reaction(s) or only histidinol dehydrogenase, or both. Those that lack only histidinol dehydrogenase accumulate histidinol (16, 162, 1123). Mutants produce cross-reacting material (220). Used to study intralocus complementation and recombination (15, 16, 27, 162, 164, 171, 172, 1121, 1122, 1124). Intralocus recombination is regulated by cog and by rec-2 (27, 171); it is not affected by rec-1 (172). Translocation T(IR;VII)TM429, with one breakpoint in his-3, has been used to show that cog is cis-acting (171). Initial alleles: C140 and T1710 (= C1710).	IR	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
mtr	IVR. Between pdx-1 (2%) and col-4 (1%) (101, 1017).Resistant to 4-methyltryptophan and p-fluorophenylalanine. pmn (= Pm-N, pm n), selected by resistance to p-fluorophenylalanine, has been shown to be alletic with mtr(R. Sadler and S. Ogilvie-Villa, personal communication; see also reference 248). Defective in transport of neutral aliphatic and aromatic amino acids via amino acid transport system I (as defined in reference 777) (248, 602, 1017, 1152). Causes an alteration in surface glycoproteins (1038). Used extensively for transport studies (247a, 1150 [review], 1152), also for studies of the mechanism of intralocus recombination (1021). Resistance is recessive in duplications from T(S1229) (PB). Recessive resistance used in a heterokaryon test system for mutation studies (1020). Suppressors obtained and used for selecting other resistance mutants (106, 107, 555, 1018). Allele 26 is a putative frameshift mutation reverted by ICR170 (106, 107). mtrascospores are slow to darken and mature; up to 50% of the young ascospores from heterozygous crosses are white (152, PB). With probable allele MN18, ascospore viability is improved by the addition of peptone to the crossing medium when the male parent is added (152). mtr has been scored on media containing 10 or 70 µg of filter-sterilized 4-methyltryptophan per ml or on 20 or 60 µg of p-fluorophenylalanine per ml (550, 1021, PB). Unlike 4-methyltryptophan, p-fluorophenylalanine is heat stable and can be added before autoclaving. Strains with mutations at the mtr locus may be obtained by selection for resistance to numerous agents or for defects in uptake ability. Thus, there is confusion in nomenclature. Genes originally designated neua, neur, neut, tru(628) may be mtr alleles. mtr was initially called mt (602).	IVR	B