FGSC #9416 Species: Neurospora crassa
Genotype: col-16;pk
Alleles: R2539,B6
Linkage Group(s): IIIR,VR
Stock No. from Other Collection: OG51
Depositor of Strain: OG
Lesion: col-16 colonial-16
Lesion Information for Marker:
      Linkage Group of col-16: IIIR
      Markers Left of col-16: Linked to leu-1 (1%) and pro-1 (10%)
Marker description or requirements:
      IIIR. Linked to leu-1 (1%) and pro-1 (10%) (382; PB).Colonial morphology (382). Forms balls of powdery conidia at top of slants of glycerol complete medium. A good marker, preferable to com; strains carrying the latter grow more slowly and do not conidiate (PB). Complements mo-4 and spco-15 (382).
Reference for: col-16: 382. Garnjobst, L. , and E. L. Tatum. 1967. A survey of new morphological mutants in Neurospora crassa. Genetics 57:579-604.
Lesion: pk peak (synonym
Enzyme Name: L-glutamine D-fructose-6-phosphate amidotransferase
Marker description or requirements:
      bis, biscuit) VR. Between met-3 (1%) and T(EB4)^L, cot-2 (8%), cl (2%). Growth on an agar surface is initially colonial and flat. A mass of aerial hyphae is then sent up, which conidiates profusely (1548). Somewhat similar in morphology to sn, cum, sp, and cot-4 at 25ºC, but distinguishable. Hyphae branch dichotomously (1405, 1548). Increased activity of L-glutamine:D-fructose-6-phosphate amidotransferase was observed in crude extracts of one pk strain, but not in nine others; increased activity for this enzyme also was found in cl and in four other nonallelic morphological mutants (1758). Hexoseaminoglycan consists of a single component on medium without sorbose, in contrast to two components in wild type (1960). Antigenic surface mucopolyoside (532). Cell-wall analysis and photograph, allele B6 (507) and allele C-1810-1 (287). Cell-wall enzymes (633). Effect of carbon source (531). One observation suggested a functional interaction with cl (1965), but substantial crossing-over frequencies and recovery of the double mutant pk cl indicated that the loci are distinct (569). The gene was named for the vegetative mutant phenotype, which is recessive. Several alleles were called bis (1592). The sexual phase is also affected. Asci are thin-walled, bulbous, and nonlinear in homozygous pk ´ pk crosses (1406, 1409, 1550). Spindle orientation is abnormal in the swollen asci, and no apical pore is formed (1625, 1679). Most mutant alleles are recessive for the ascus effect, but some are dominant with variable penetrance. Sorbose-resistant mutants at various loci act as dominance modifiers of the ascus effect of dominant alleles (1757). Sexual-phase-recessive allele C-1610 and dominant allele 17-088 are both associated with reciprocal translocations (1578).


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