Recombinational landscape across a 650-kb contig on the right arm of linkage group V in Neurospora crassa

1999 ◽  
Vol 36 (5) ◽  
pp. 270-274 ◽  
Author(s):  
Frederick J. Bowring ◽  
David E. A. Catcheside
Genetics ◽  
1976 ◽  
Vol 82 (1) ◽  
pp. 9-17 ◽  
Author(s):  
Jerry F Feldman ◽  
Marian N Hoyle

ABSTRACT A fourth mutant of Neurospora crassa, designated frq-4, has been isolated in which the period length of the circadian conidiation rhythm is shortened to 19.3 ± 0.3 hours. This mutant is tightly linked to the three previously isolated frq mutants, and all four map to the right arm of linkage group VII about 10 map units from the centromere. Complementation tests suggest, but do not prove, that all four mutations are allelic, since each of the four mutants is co-dominant with the frq  + allele—i.e., heterokaryons have period lengths intermediate between the mutant and wild-type—and since heterokaryons between pairs of mutants also have period lengths intermediate between those of the two mutants.


Genetics ◽  
1994 ◽  
Vol 136 (4) ◽  
pp. 1297-1306
Author(s):  
C R Davis ◽  
R R Kempainen ◽  
M S Srodes ◽  
C R McClung

Abstract We have cloned three linked genes serine-1 (ser-1), proline-1 (pro-1) and acetate-2 (ace-2) that lie near the centromere on the right arm of linkage group III (LGIIIR) of Neurospora crassa. The ser-1 gene was cloned by sib selection. A chromosomal walk that spans 205 kilobases (kb) was initiated from ser-1. Complementation analysis with clones isolated during the walk allowed identification of the pro-1 and ace-2 genes. Restriction fragment length polymorphism analysis has confirmed the localization of ser-1, pro-1 and ace-2 to the centromeric region of LGIIIR. Genetically, we measured 1% recombination between ser-1 and pro-1 and 2% recombination between pro-1 and ace-2. Physical distances for these intervals were 114 kb from ser-1 to pro-1 and 36 kb from pro-1 to ace-2. Thus, for the pro-1 to ace-2 interval we calculate a physical/genetic correlation of 18 kb/map unit (mu) whereas, in the immediately adjacent, centromere-proximal interval from ser-1 to pro-1, we calculate 114 kb/mu. This provides evidence for a centromere effect, a decrease in recombination frequency as one approaches the centromere.


1970 ◽  
Vol 23 (5) ◽  
pp. 1229 ◽  
Author(s):  
Teresa Angel ◽  
Barbara Austin ◽  
DG Catcheside

The frequency of prototrophic recombination between pairs of his-3 alleles is increased in the absence of the dominant gene reo-w+, which is probably the same as reo-4+. The locus of reo-w is in linkage group V. The degree of increase is determined by genes at a reoognition locus (oog) situated about 1� 3 units distally to the hi8-3 locus. In the presence of oog+, derived from Y8743 which has Lindegren wild stocks as ancestors, the increase is about 30-fold.


1968 ◽  
Vol 10 (2) ◽  
pp. 351-356 ◽  
Author(s):  
R. E. Subden ◽  
S. F. H. Threlkeld

A spontaneously occurring mutant called "yellow b" has been isolated and mapped on the right arm of linkage group I in Neurospora crassa 0.15 c.o.u. distal to aur and 2 c.o.u. distal to al-2. These three markers complement each other and are involved in the same biosynthetic pathway.


1985 ◽  
Vol 5 (6) ◽  
pp. 1301-1306
Author(s):  
P Eversole ◽  
J J DiGangi ◽  
T Menees ◽  
R H Davis

To define the structural gene for ornithine decarboxylase (ODC) in Neurospora crassa, we sought mutants with kinetically altered enzyme. Four mutants, PE4, PE7, PE69, and PE85, were isolated. They were able to grow slowly at 25 degrees C on minimal medium but required putrescine or spermidine supplementation for growth at 35 degrees C. The mutants did not complement with one another or with ODC-less spe-1 mutants isolated in earlier studies. In all of the mutants isolated to date, the mutations map at the spe-1 locus on linkage group V. Strains carrying mutations PE4, PE7, and PE85 displayed a small amount of residual ODC activity in extracts. None of them had a temperature-sensitive enzyme. The enzyme of the PE85 mutant had a 25-fold higher Km for ornithine (5mM) than did the enzyme of wild-type or the PE4 mutant (ca. 0.2 mM). The enzyme of this mutant was more stable to heat than was the wild-type enzyme. These characteristics were normal in the mutant carrying allele PE4. The mutant carrying PE85 was able to grow well at 25 degrees C and weakly at 35 degrees C with ornithine supplementation. This mutant and three ODC-less mutants isolated previously displayed a polypeptide corresponding to ODC in Western immunoblots with antibody raised to purified wild-type ODC. We conclude that spe-1 is the structural gene for the ODC.


Genetics ◽  
1967 ◽  
Vol 57 (3) ◽  
pp. 605-612 ◽  
Author(s):  
M P Morgan ◽  
L Garnjobst ◽  
E L Tatum

1969 ◽  
Vol 60 (3) ◽  
pp. 120-125 ◽  
Author(s):  
EDWARD G. BARRY ◽  
DAVID D. PERKINS

Genetics ◽  
1990 ◽  
Vol 124 (3) ◽  
pp. 615-625
Author(s):  
R E Rosenbluth ◽  
R C Johnsen ◽  
D L Baillie

Abstract The effect of deficiencies on recombination was studied in Caenorhabditis elegans. Heterozygous deficiencies in the left half of linkage group V [LGV(left)] were shown to inhibit recombination to their right. Fourteen deficiencies, all to the left of unc-46, were analyzed for their effect on recombination along LGV. The deficiencies fell into two groups: 10 "major inhibitors" which reduce recombination to less than 11% of the expected rate between themselves and unc-46; and four "minor inhibitors" which reduce recombination, but to a much lesser extent. All four minor inhibitors delete the left-most known gene on the chromosome, while six of the ten major inhibitors do not (i.e., these are "internal" deficiencies). Where recombination could be measured on both sides of a deficiency, recombination was inhibited to the right but not to the left. In order to explain these results we have erected a model for the manner in which pairing for recombination takes place. In doing so, we identify a new region of LGV, near the left terminus, that is important for the pairing process.


Genetics ◽  
1988 ◽  
Vol 119 (4) ◽  
pp. 805-814
Author(s):  
R Benarous ◽  
C M Chow ◽  
U L RajBhandary

Abstract We generated a lambda gt11 Neurospora crassa cDNA library and screened the library for the cytoplasmic leucyl-tRNA synthetase (cyto LeuRS) clones using cyto LeuRS specific antibody. Two clones, lambda NCLRSC1 and lambda NCLRSC2, were obtained which have inserts of approximately 2 kbp and approximately 1.3 kbp, and which overlap by about 0.6 kbp. The following lines of evidence indicate that lambda NCLRSC1 and lambda NCLRSC2 encode parts of cyto LeuRS. (1) Antibodies affinity purified using either of the fusion proteins encoded by lambda NCLRSC1 or lambda NCLRSC2 inhibit cyto LeuRS activity. Thus, the fusion protein and cyto LeuRS share immunological determinants. (2) The same antibodies also react with an approximately 115-kDa protein, which comigrates with purified cyto LeuRS, in immunoblots of total N. crassa proteins. We used the cDNA clones to probe a N. crassa genomic DNA library and isolated two genomic DNA clones. Partial sequence analysis of cDNA and genomic DNA clones shows a methionine initiated open reading frame, which includes a stretch of amino acid residues that are highly conserved and that are at the ATP binding site in aminoacyl-tRNA synthetases. Using the cloned DNA as probe, we show that the cyto LeuRS mRNA is approximately 3900 nucleotides long. Finally, we have used restriction fragment length polymorphism mapping to show that the cyto LeuRS gene resides on the far right of linkage group II and not on linkage group V where the leu-5 mutation, which was previously reported to specify cyto LeuRS, is located.


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