FGSC #235

Mutant Type

Genus: N

reporting_genes: ad-5 his-2 al-1 pt ylo-1

species: Neurospora crassa

allele: Y152M40 Y152M14 34508;NS/t;Y30539

stock: 1286

glasgow:

mutagen:

Depositor: DDP

Link Group: IL IR IR;IVR;VIL

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-235

ksudc_link_html: https://digital.lib.k-state.edu/item/neurospora-crassa/fgsc-235 ↗

Genes

Locus	Cultural Requirements	Link Group	Type
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
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 (797, 808; D.D. Perkins, unpublished data).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
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
pt	IVR. Right of T(S1229) and pdx-1 (2%). Left of col-4(2%) (40, 55, 808). (201) Original S4342 strain contained linked but separable insertional translocation T(S4342) (808), the presence of which should not change conclusions regarding gene order given in reference 40. Requires phenylalanine plus tyrosine (201). Lacks chorismate mutase (40, 316) (Fig. 11). Evidently the structural gene; strains carrying allele NS1 have thermolabile chorismate mutase (D.E.A. Catcheside, personal communication). NS1 strains are temperature sensitive, growing on minimal medium at 25 C, where they are readily scorable by blue fluorescence under long-wave UV and by browning of medium of aging cultures (1035). Inhibited by complex complete medium.	IVR	B
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