FGSC #5196

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Reporting Genes: sn cr-1;cyh-2 al-3 inl;nic-3 met-7 arg-10

Species: crassa

Allele: C136 B123 KH53(r) RP100 83201t H193 Y31881 48941 B317

Alternate Strain Number: M2012

Depositor: EK

Linkage Group: I IR;VR VR VR;VIIL VIIR VIIR

Mating Type: a

Species Number: 10

Deposit Sheet ↗

Genes

Locus	Cultural Requirements	Link Group	Type
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83201 show slow semicolonial growth in liquid minimal medium at 25°C (641), but look normal on slants (D.D. Perkins, unpublished data).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
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
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
arg-10	Uses arginine but not precursors.	VIIR	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-2	VR. Right of lys-2 (<1%). Left of leu-5 (<1 to 2%) and sp(2 to 9%) (496, 818, PB). Resistant to cycloheximide (496, 748). Protein synthesis on mutant ribosomes proceeds in the presence of cycloheximide in a cell-free system (834). Excellent marker. Readily scored on slants with 10 µg of cycloheximide per ml autoclaved in the medium or with 1 µg added after autoclaving. Resistance in heterokaryons has been reported to be dominant (496, 626) or recessive (939); it may depend on nuclear ratios or media. Used in mutagenicity test systems (626). Used to show that the cycloheximide-induced phase shift of the circadian clock involves protein synthesis (738). Double mutant cyh-1;cyh-2grows slowly and is much more insensitive to cycloheximide than either single mutant (496).	VR	B