FGSC #7277

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Reporting Genes: met-7;am132 inl inv mei-2

Species: crassa

Depositor: RLM

Mating Type: a

Species Number: 10

Deposit Sheet ↗

Genes

Locus	Cultural Requirements	Link Group	Type
mei-2	VR. Linked near inl (995). Between al-3 (20 and his-6(A.L. Schroeder, personal communication). Meiotic divisions occur, and many ascospor are produced, but many are inviable and white. Crosses heterozygous or homozygous for Mei-2 give extensive nondisjunction of all linkage groups (995). Chromosome pairing much reduced (B.C. Lu, cited in reference 995). Sensitive to methyl methane sulfonate, histidine, and gamma rays (939). Dominant in the original strain (995), but progeny show incomplete penetrance (939).	VR	B
met-7	VIIR. Right of qa-2 (<1%), ars (<1%), and the centromere (one second-division ascus in several hundred). Left of met-9 (10[-4]) and wc-1 (1 to 4%) (146, 725; M.E. Case, personal communication). (718; M.K. Allen, cited in references 718 and 789) Uses cystathionine, homocysteine, or methionine (718; N. H. Horowitz, cited in reference 1180). Lacks cystathionine-gamma-synthase (547) (Fig. 17). This enzyme is also lacking in the mutant met-3 (547). See met-3 for regulation. Apparently contiguous with met-9by coconversion. Flanking markers are recombined in most met-7+ met-9+ recombinants (725). Functionally distinct from the mutant met-9, which has active cystathionine-gamma-synthase (547) but cannot use homocysteine. No mutants lacking both functions have been isolated. Allele NM251 is suppressible by supersuppressor RN33 (same as ssu-1?) (725). Allele K79 is inseparable from reciprocal translocation T(I;VII)K79 (808).	VIIR	B
inl	VR. Between pho-3 (3 to 4%) and pab-1 (1 to 10%). Right of al-3 (362, 397, 1036). (482)Requires inositol (65). Lacks D-myoinositol-1-phosphatase (1142). Lack of glucocycloaldolase found by Pina and Tatum (826) is attributed by Williams (1142) to drastic repression of glucocycloaldolase by the concentration of inositol used for growth. Growth is colonial on low levels of inositol (367). Tends to extrude dark pigment into the medium when grown on suboptimal inositol. Composition of phospholipids and cell walls is abnormal on limiting inositol (367, 439, 440, 501). Inhibited by hexachlorocyclohexane (366, 457, 931). Conidia are subject to death by unbalanced growth on minimal medium (1028, 1033), a property exploited for mutant enrichment ("inositol-less death") (606, 647) because double mutants are at a selective advantage. Heat-sensitive allele 83201 is especially useful for mutant enrichment (832, 1043). Used in the first experiments reporting transformation of Neurospora by N. crassaDNA (677, 679) and reported to be efficient as a recipient in absence of inositol (1162). Used to study glucose (917) and sulfate (641) transport systems. Used extensively for studying induced reversion (392). Used for studying the mechanism of inositol-less death (647, 702), mutagenicity of ferrous ions, and regulation of mitochondrial membrane fluidity; for a review, see reference 702. Spontaneous reversion rates (386). Allele-specific partial suppressor (390). Allele 46802 is nonrevertable and inseparable from translocation 46802 (386, 808). Strains carrying heat-sensitive allele 83201 show slow semicolonial growth in liquid minimal medium at 25°C (641), but look normal on slants (D.D. Perkins, unpublished data). Strains carrying allele 89601 contain cross-reacting material (1183). Mutant gene exo-1 is present in the inl(89601) a stock FGSC 498 and may, therefore, be present in stocks of mutants derived by inositol-less death. (See references 194, 325, and 1027). Called inos.	VR	B
am132			B
inv	VR. Right of pab-2 (3%) and ro-4 (5 to 8%), Left of asn (4 to 9%) (918, PB).Unable to use sucrose as a carbon source. Grows well on glucose or fructose and fairly well on Casamino Acids or yeast extract. Invertase structural gene; invertase deficient and uninducible by normal inducers. Makes cross-reacting material (919). Invertase is also affected by cot-2, q.v.	VR	B