FGSC #5215

Mutant Type

Genus: N

reporting_genes: sn cr-1;lys-1;ylo-1 pan-2;nic-3 met-7

species: Neurospora crassa

allele: C136 B123 33933 Y30539y Y154M64 Y31881 4894

stock: M2056

glasgow:

mutagen:

Depositor: EK

Link Group: I IR;V;VIL;VIR;VIIL VIIR

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-5215

ksudc_link_html: https://digital.lib.k-state.edu/item/neurospora-crassa/fgsc-5215 ↗

Genes

Locus	Cultural Requirements	Link Group	Type
pan-2	VIR. Right of rib-1 (<1 to 3%). Left of del (6%) and trp-2(11%) (140, 141, 143, 818, PB). Unable to convert ketovaline to ketopantoic acid (138, 140, 141). Used in major studies of intralocus recombination and complementation (140-143). pan-2ascospores remain white or pale if the crossing medium is not supplemented, even when the protoperithecial parent is pan-2+. Asci in which gene conversion has occurred at pan-2 can thus be recognized and isolated (1072, 1073); photographs (1072). For good recovery of pan-2progeny, crossing media should be supplemented with pantothenic acid (10 µg/ml) even when the protoperithecial parent is pan+. Called group B.	VIR	B
sn	I. Right of T(39311) and arg-3 (1 to 6%). Left of T(AR173) and his-2 (<1 to 12%) (174, 808). (687) Spreading colonial growth with good conidiation. Linear growth is less than 1/10 that of the wild type (19). Detectable immediately after ascospore germination by hyphal patterns which suggested the name (688). Abnormal microfilaments (19). Contains actin-like protein (20). Said not to exhibit cytoplasmic streaming (18). Meiosis and ascospore formation are normal in homozygous sn x sn crosses (N.B. Raju, personal communication). Good female fertility. Morphology similar to that of sp, cum, and cot-4mutants (at 25 C) (PB). Used to study development of crystalline inclusions (17). The cr sn double mutant grows as small, discrete, conidiating colonies suitable for velvet replication. The double mutant cr snresembles the rg cr double mutant phenotypically and has the advantage of fertility in homozygous crosses (796); for example of application, see reference 180.	IR	B
nic-3	VIIL. Right of spco-4 (1%) and do (3%). Left of thi-3 (9 to 27%) and csp-2 (16 to 22%) (539, 812, 816, PB). (M.K. Allen, cited in references 718 and 789) Uses nicotinic acid, nicotinamide, 3-hydroxyanthranilic acid, 3-hydroxykynurenine, or high concentrations of quinolinic acid (96, 1168). Accumulates alpha-N-acetylkynurenine; blocked in conversion of kynurenine to 3-hydroxykynurenine (1168) (Fig. 18). Pyridine nucleotide levels (111). Pathway from tryptophan to nicotinic mononucleotide, showing sites of gene action (96, 100, 368, 1168). The enzymatic reactions between 3-hydroxyanthranilate and nicotinic mononucleotide have not been demonstrated directly in Neurospora.	VIIL	B
met-7	VIIR. Right of qa-2 (<1%), ars (<1%), and the centromere (one second-division ascus in several hundred). Left of met-9 (10[-4]) and wc-1 (1 to 4%) (146, 725; M.E. Case, personal communication). (718; M.K. Allen, cited in references 718 and 789) Uses cystathionine, homocysteine, or methionine (718; N. H. Horowitz, cited in reference 1180). Lacks cystathionine-gamma-synthase (547) (Fig. 17). This enzyme is also lacking in the mutant met-3 (547). See met-3 for regulation. Apparently contiguous with met-9by coconversion. Flanking markers are recombined in most met-7+ met-9+ recombinants (725). Functionally distinct from the mutant met-9, which has active cystathionine-gamma-synthase (547) but cannot use homocysteine. No mutants lacking both functions have been isolated. Allele NM251 is suppressible by supersuppressor RN33 (same as ssu-1?) (725). Allele K79 is inseparable from reciprocal translocation T(I;VII)K79 (808).	VIIR	B
lys-1	V. Right of caf-1 (4 to 14%). Left of cyt-9 (5%) and at (1 to 20%) (817; K.S. Hsu, personal communication; PB). (403)Uses lysine, alpha-aminoadipic acid, or epsilon-hydroxynorleucine (alpha-amino-epsilon-hydroxycaproic acid) (399, 400, 684, 1087). Accumulates homocitrate on limiting lysine concentrations (464) (Fig. 16). Fine structure and complementation between alleles (8). Initial allele: 33933.	V	B
cr-1	IR. Right of ace-7 (1 to 3%) and nic-2 (4 to 7%). Left of cys-9 (3%) and un-1(5%) (721, 816). Included in duplications from T(4540), which do not include cr-2 or cr-3(PB). (610) Rapid conidiation close to surface of agar. Produces very short conidiophores, bearing conidia in tight clusters (610, 611). Photographs (533, 634). Recessive. Deficient in adenylate cyclase (1066); has little or no endogenous adenosine 3',5'-phosphate (1065, 779). Abnormal morphology partially corrected by exogenous adenosine 3',5'-phosphate (891, 892, 1065, 1066). Guanosine 3',5'-phosphate also stimulates mycelial elongation (892). Cyclic nucteotide levels differ in mycelia and conidia (891, 892). NAD(P) glycohydrolase is overproduced and excreted; this is normalized by adenosine 3',5'-phosphate (533). Induction and localization of p-glucosidase is altered; induction is normalized by adenosine 3',5'-phosphate (906). Inability to use glycerol and certain other carbon sources is also overcome by adenosine 3',5'phosphate (598, 1067). Phosphodiesterase inhibitors do not counteract the morphological effect of cr-1 (892). Increased lactate dehydrogenase activity (92). Used to determine what functions are controlled by adenosine 3',5'-phosphate (779). Used to study adenosine 3',5'-phosphate binding protein (1082). Strains carrying the various alleles vary in growth habit (B123 strains are flat, restricted; allele L strains are spreading, but morphology may vary on different media). Modifier mutations which alter morphology and the ability of cr-1 to use glycerol occur frequently (383, 905). Crosses homozygous for allele B123 exude intact linear asci (634). Double mutants sn cr and cr rg form small conidiating colonies suitable for replica plating with velvet (182, 634, 796, 932, 1020). The triple mutant sn cr;csp-2 can be overlayered (744; photograph 747). The single mutant (B123) can be replicated by using a needle replicator (634). Scorability and viability are good. Excellent as a marker. Carotenoids formed normally. cr-1 ascospores may require longer to mature than cr+ ascospores. Allele CE4-11-67 called con(716, 717).	IR	B
ylo-1	VIL. Between cys-1 (8%) and ad-1 (6%). Probably right of Bml (2%) (1012, PB). (381). Yellow carotenoids (381). Affects synthesis of neurosporaxanthin (4'-apo-beta'-caroten-4'-oic acid); citations in reference 398. Lesion probably involves the conversion of lycopene to 3,4-dehydrolycopene or the conversion of either torulene or gamma-carotene to neurosporaxanthin (398 and references therein) (Fig. 9). Resembles the orange wild type in young cultures, but color differences become clear with age. Expressed in both conidia and mycelia. Undefined modifiers affect intensity. Fails to complement with many of the al-1 and al-2 albino strains (R.E. Subden, personal communication).	VIL	B