FGSC #7280

Mutant Type

Genus: N

reporting_genes: ad-1;am132 inl inv mei-1

species: Neurospora crassa

allele:

stock:

glasgow:

mutagen:

Depositor: RLM

Link Group:

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-7280

ksudc_link_html: https://digital.lib.k-state.edu/item/neurospora-crassa/fgsc-7280 ↗

Genes

Locus	Cultural Requirements	Link Group	Type
ad-1	VIL. Right of ylo-1 (6%). Left of the centromere (< 1 to 2%), T(AR209), and rib-1(3 to 5%) (1102, 1012). (482) Uses adenine or hypoxanthine (682, 824). Accumulates AICAR (81, 904) and SAICAR (81). May affect inosine 5'-monophosphate cyclohydrolase (902, 904) (Fig. 8). Used to study purine transport (903 and references therein). Ascospores are white in homozygous ad-1 x ad-1 crosses, and ad-1 ascospores may be white in heterozygous crosses (D.D. Perkins, unpublished data). Called complementation group M.	VIL	B
am132			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
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
mei-1	IVR. Linked to arg-2 (<1%), probably to the right (995). Meiosis is impaired in homozygous crosses. Recessive. Meiotic divisions occur and many ascospores are produced, but 70 to 90% are inviable and white. The viable ascospores are usually disomic for one or more linkage groups, indicating high nondisjunction at the first division (254, 995). Chromosome pairing is defective: axial elements of synaptonemal complex are present, but a completed complex is rarely seen. Separation at anaphases I and II is defective, leading to four-poled second and third division spindles (625). Not sensitive to UV, methyl methane sulfonate, ionizing radiation (939), or histidine (939; D. Newmeyer, unpublished data). mei-1 is present in wild-collected strain Abbott 4A (995), which is an ancestor of many Beadle and Tatum mutants (68). Possible allele asc(DL243)complements mei-1 but did not recombine with it (0/3,000) (253). DL243 and mei-1 strains differ phenotypically. In DL243 mutants, the major block is before karyogamy; the few asci produced have normal meiosis I but high nondisjunction at meiosis II, with most chromosomes usually attached to only one spindle-pole body (254). Possible allele asc(DL95) complements mei-1 and asc(DL243), but did not recombine with DL243 (0/96) (253). DL95 is phenotypically like mei-1 but is less extreme (254).	IVR	B