FGSC #246

Mutant Type

Genus: N

reporting_genes: ad-5 his-2 cr-1

species: Neurospora crassa

allele: Y152M40 Y152M14 B123

stock: 1278

glasgow:

mutagen:

Depositor: DDP

Link Group: IL IR IR

MT: a

Species No: 10

gene_back:

oppmt: 0

trans:

ref1: Catcheside, D.E.A. Aust. J Biol Sci 27:563 (1974), https://doi.org/10.1071/BI9740561

ref2:

site:

country:

ksudc_link: https://digital.lib.k-state.edu/item/neurospora-crassa/fgsc-246

ksudc_link_html: https://digital.lib.k-state.edu/item/neurospora-crassa/fgsc-246 ↗

Genes

Locus	Cultural Requirements	Link Group	Type
ad-5	IL. Between phe-1 and arg-1 (1%) (816; H.B. Howe, Jr., personal communication). (482) Uses adenine or hypoxanthine (682) (Fig. 8). Accumulates AICAR (81, 904) and SAICAR (81). Some mutants are stimulated by histidine and may not grow on hypoxanthine unless histidine is present; others may be inhibited by histidine (393; M.E. Case, personal communication). Produces some purple pigment, but less than ad-3A and ad-3Bmutants (526). Called complementation group J. Evidence, apparently enzymatic, given in reference 120 suggests that some ad-5 mutants lack both AICAR formyltransferase and inosine 5'-monophosphate cyclohydrolase, but apparently other ad-5 mutants lack only the formyltransferase. Indirect evidence (902, 904) suggests that strains carrying ad-5 allele Y112M192 are blocked at the formyltransferase step.	IL	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
his-2	IR. Right of T(AR190) and un-2 (<1%). Left of the T(AR173) right breakpoint and of nuc-1 (<1%) (172, 670, 808). (434)Requires histidine (434). Affects adenosine 5'-triphosphate phosphoribosylpyrophosphate pyrophosphorylase (16) (Fig. 14). Intralocus complementation (162). Recombination between his-2 alleles is controlled by rec-3(173); it is not affected by rec-1 (172). Initial his-2 allele called C94.	IR	B