FGSC #5192

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Reporting Genes: sn cr-1;lys-1 cyh-2 al-3 inl(ts)pab-2

Species: crassa

Allele: C136 B123 33933 KH53(r) RP100 83201t H193

Alternate Strain Number: M1860

Depositor: EK

Linkage Group: I IR;V VR VR VR VR

Mating Type: A

Species Number: 10

Opposite Mating Type: 5193

Deposit Sheet ↗

Genes

Locus	Cultural Requirements	Link Group	Type
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
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
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
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
pab-2	VR. Right of ad-7 (8%). Left of inv (3%) and asn (1 to 15%). Linked to ro-4(0/407) (156, 816, 818, 918, 1036). (47) Requires p-aminobenzoic acid (1182) (Fig. 11). Allele 71301 called pab-3(1182); shown to be allelic by Drake (289).	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
inl(ts)	Requires inositol, Temp Sensitive	VR	B