FGSC #4562

Mutant Type

Genus: n

reporting_genes: (col-2A + a[m1] ad-3B cyh-1)

species: Neurospora crassa

allele: Y5331 + 1 B114 KH52

stock: 7182=7180

glasgow:

mutagen:

Depositor: DDP

Link Group:

MT: A

Species No: 10

gene_back:

oppmt: 4563

trans:

ref1: https://doi.org/10.1093/genetics/88.2.239

ref2:

site:

country:

ksudc_link: https://digital.lib.k-state.edu/item/neurospora-crassa/fgsc-4562

ksudc_link_html: https://digital.lib.k-state.edu/item/neurospora-crassa/fgsc-4562 ↗

Genes

Locus	Cultural Requirements	Link Group	Type
ad-3	IR. Between his-3 (1 to 2%) and ad-3B (0.1 to 0.7%) (271). Right of ure-4 (78). (482) Requires adenine or hypoxanthine (682). Blocked in interconversion of CAIR plus aspartate to SAICAR (348) (Fig. 8). Produces purple pigment, permitting direct visual selection (276, 682); see the ad-3B entry. Reduced interallelic fertility (407). No interallelic complementation (267; F.J. de Serres, personal communication). ad-3A and ad-3B are two genetically and functionally distinct loci separated by a short but functionally complex region of unknown but essential function (271, 407). They have been used intensively for quantitative genetic and molecular studies of mutation (for a review, see reference 35). Either forward mutation (e.g., reference 277) or reverse mutation (e.g., reference 772) can be measured precisely; the former is detected visually by purple pigment. Purple pigment has also been used to assess the effect of histidine and tryptophan on purine nucleotide synthesis (786). Alleles N23 and N24 have been used as mutagen testers. N23 reverts with agents that cause base pair substitutions; N24 reverts with agents that cause frameshifts (772). SK(ad-3A) is at or near ad-3A and may be a cryptic ad-3A allele. Does not require adenine. In SK(ad-3A)x ad-3Acrosses, the ad-3A progeny die; possibly SK(ad-3A) mutants fail to make enough adenine to support their growth (251). Translocations Y155M64 ad-3A (272; PB) and Y112M15 ad-3A(413) each have one breakpoint that is inseparable from ad-3A. Called complementation group A (264). "A" in the locus symbol does not refer to mating type.	IR	B
cyh-1	IR. Right of nit-1 (6%). Left of T(STL76) and al-2 (8 to 13%) (496, 797, 808).Resistant to cycloheximide (496, 748). Resistance is recessive in duplications (1090). Dominance reported in forced heterokaryons (496, 748) may have been due to skewed nuclear ratios (1090). Protein synthesis on ribosomes of the mutant cyh-1 proceeds in the presence of cycloheximide in a cell-free system (834). Readily scored on slants with 10 µg of cycloheximide per ml autoclaved in the medium. Excellent as a marker and valuable for selecting somatic recombinants or deletions in heterozygous duplications (748, 1091). Used to show that the cycloheximide-induced phase shift of the circadian clock involves protein synthesis (738). Called act-1: actidione resistant-1.	IR	B
am1			B
col-2	VII. Linked to met-7 and met-9 (1%), probably to the left (812, 816). Right of T(T54M50) (D.D. Perkins, unpublished data). Colonial morphology (46). Photographs (112, 9469 948). Altered structure of NADP-specific glucose-6-phosphate dehydrogenase (116, 949). (bal and frmutants are also deficient in glucose-6-phosphate dehydrogenase.) Reduced NADPH level (110). Reduced linolenic level (115). Accumulates much neutral lipid (765). Pyridine nucleotide levels (111). Suppressor su(col-2)increases the linear growth rate and influences the electrofocusing pattern of col-2 glucose-6-phosphate dehydrogenase (948). Homozygous col-2x col-2crosses fail to mature. Immature asci are frequently nonlinear and occasionally show dichotomization (1007). Hyphae swell with age to diameters of 20 um (197).	VII	B