FGSC #2565

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Reporting Genes: rec-2;cog;cot-1;his-3 ad-3

Species: crassa

Allele: no#;no#;C102(t);K874 K118

Alternate Strain Number: 7448

Depositor: DGC

Linkage Group: VR;IR;IVR;IR IR

Mating Type: A

Species Number: 10

ref1: https://doi.org/10.1071/bi9740561; https://doi.org/10.1071/bi9740219

ref2: https://doi.org/10.1071/bi9710107

Deposit Sheet ↗

Genes

Locus	Cultural Requirements	Link Group	Type
cog	IR. Between his-3 (1 to 3%) and ad-3A (2 to 7%) (27, 171). The postulated site for initiating local recombination in meiosis. Affects recombination in adjoining regions, in the absence of rec-2+. Presence of cog+ then increases recombination within his-3 (27) and crossing over between his-3 and ad-3 (171). The allele for high recombination is completely dominant, and its effect is specifically on the his-3 alleles in chromatids that contain cog+, as evidenced by crosses heterozygous for reciprocal translocation TM429, which has a breakpoint between sites within the his-3 locus (171). See rec and rec-2; see Fig. 22.	IR	B
rec-2	VR. Between sp and am (174). (993) Presence of dominant allele rec-2+ reduces recombination within the his-3locus (IR); also reduces crossing over in the intervals pyr-3-his-5(IVR), his-3-ad-3 (IR), and arg-3-sn (IL) (171, 74, 992) (Fig. 22). Interacts with cog in affecting recombination in his-3 and crossing over between his-3and ad-3 (27, 171). Used in conjunction with translocation TM429to demonstrate the cis action of cog+ on recombination between sites in his-3(171). (See cog.) Recessive rec-3 alleles from other lineages were called rec-4, rec-5, or rec-w until identity was demonstrated (see reference 167). Map locations of the rec genes. Arrows show the sites where they are known to affect meiotic intra- or interlocus recombination frequencies, and the magnitude of the effect (170 and references therein; D.E.A. Catcheside, personal communication).	VR	B
cot-1	IVR. Between pan-1 (2%) and his-4 (1 to 6%) (692, 812, 816). Extremely colonial at 34°C, but completely normal growth, morphology, and fertility at 25°C and below. Linear growth is maximum at 24°C (374). Becomes colonial at 32°C; colonies from ascospores or conidia are viable and continue to grow slowly with dense branching, but do not conidiate. They quickly resume normal growth when shifted to a permissive temperature (692, 1068). Recessive in duplications (808); apparent dominance in heterokaryons (374) may have resulted from a shift in nuclear ratios. Used in studies of septation and branching (202), growth-inhibiting mucopolysaccharide (878, 879), and sulfate transport (641). Cell wall analysis (374). Growth is stimulated by lysine or arginine (0.1 mM) on glucose media at high temperatures (615). Because of high viability and tightly restricted growth at restrictive temperatures and normality at 25°C, cot-1 mutants have valuable technical applications. For example, crosses homozygous for cot-1 have been used in combination with sorbose for experiments with rec genes, where high-density ascospore platings are required for precise quantitative analysis of intralocus recombination (e.g., references 165, 997, and 1070). In another application, when shifted up after initial growth at the permissive low temperature, cot-1hyphae assume a "bottle brush" appearance with small side branches (692). This has been used to select uvs mutants by subsurface survival on UV-irradiated plates containing p-aminobenzoic acid (938; D.E.A. Catcheside, personal communication). cot-1 conidia or ascospores from cot-1 x cot-1crosses are used for replication in a protocol involving transfer by filter paper (615). For suppressors of cot-1, see gul.	IVR	B
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
his-3	IR. Right of met-10 (R.L. Metzenberg, personal communication). Left of cog (1 to 3%) (172,174), ure-4 (1%) (78), and ad-3A (1%) (271). (434)Requires histidine (434). Complex gene coding for histidinol dehydrogenase, phosphoribosyladenosine 5'-triphosphate-pyrophosphohydrolase, and phosphoribosyl-adenosine 5'-monophosphate-cyclohydrolase (16, 673) (Fig. 14). All three activities appear to be catalyzed by a single protein (673). Strains carrying different individual alleles may lack only the early reaction(s) or only histidinol dehydrogenase, or both. Those that lack only histidinol dehydrogenase accumulate histidinol (16, 162, 1123). Mutants produce cross-reacting material (220). Used to study intralocus complementation and recombination (15, 16, 27, 162, 164, 171, 172, 1121, 1122, 1124). Intralocus recombination is regulated by cog and by rec-2 (27, 171); it is not affected by rec-1 (172). Translocation T(IR;VII)TM429, with one breakpoint in his-3, has been used to show that cog is cis-acting (171). Initial alleles: C140 and T1710 (= C1710).	IR	B