scholarly journals DUPLICATIONS IN CAENORHABDITIS ELEGANS

Genetics ◽  
1979 ◽  
Vol 92 (2) ◽  
pp. 419-435
Author(s):  
Robert K Herman ◽  
James E Madl ◽  
Claire K Kari

ABSTRACT Thirteen chromosomal duplications, all unlinked to their linkage group of origin, have been identified following X-irradiation. Ten are X-chromosome duplications, of which six are half-translocations on three autosomomal linkage groups and four are free fragments. Five of the half-translocations are homozygous fertile and two are recognizable cytologically as chromosome satellites, both of which show some mitotic instability. The free-X duplications show varying tendencies for loss. Three appear not to overlap in extent previously identified free-X duplications. The fourth carries genes from linkage group V, as well as X. Three duplications of a portion of linkage group II were identified and found to be free and quite stable in hyperploids. Some of the free duplications tend to disjoin from the X chromosome in males. New X-chromosome map data are presented.

1984 ◽  
Vol 26 (6) ◽  
pp. 762-764 ◽  
Author(s):  
Peter S. Dawson

Reindeer (Rd) is a dominant mutation affecting antenna morphology in the tenebrionid flour beetle, Tribolium castaneum. In contrast with most dominant mutants previously described for this species, homozygotes are fully viable, thus making Rd very useful for genetic studies. Rd is tentatively assigned to either linkage group IX or X. Abbreviated appendages (aa), formerly placed in linkage group X, is reassigned to linkage group V on the basis of demonstrated linkage to jet (j).Key words: Tribolium, mutation Rd, linkage, antenna morphology.


Genome ◽  
1990 ◽  
Vol 33 (1) ◽  
pp. 109-114 ◽  
Author(s):  
Denise V. Clark ◽  
Robert C. Johnsen ◽  
Kim S. McKim ◽  
David L. Baillie

A screen was conducted for lethal mutations in the nematode Caenorhabditis elegans in a strain containing the mutator mut-4(st700)I to examine the nature of mutator-induced lethal mutations within two large chromosomal regions comprising a total of 49 map units (linkage group IV (right) and linkage group V (left)). The genetic analysis of 28 lethal mutations has revealed that the mutator locus mut-4(st700)I causes both putative single-gene mutations and deficiencies. We have identified lethal mutations in three different genes, in addition to seven deficiencies. There is a mutational hot spot on linkage group V (left) around the lin-40 locus. Six mutations appear to be alleles of lin-40. In addition, 5 of 7 deficiencies have breakpoints at or very near lin-40. All seven deficiencies delete the left-most known gene on linkage group V (left) and thus appear to delete the tip of the chromosome. This is in contrast to gamma ray and formaldehyde induced deficiencies, which infrequently delete the closest known gene to the tip of a chromosome.Key words: Caenorhabditis elegans, mutator, deficiencies, lethal mutations.


1972 ◽  
Vol 19 (2) ◽  
pp. 157-164 ◽  
Author(s):  
Anne McVittie

SUMMARYEight newly isolated 9 + 0 mutants each mapped at one of the four previously known loci. Short flagellum mutants were at three loci, two of which (pf7 and pf8) were closely linked; the third, pf21, was unlinked to these two and mapped on linkage group II. The long flagellum mutants lf1 and lf2 were on linkage groups II and XII respectively. Mutants pf8A and lf1 were both recessive to wild-type. There was no evidence for non-Mendelian flagellum mutants.


1999 ◽  
Vol 77 (8) ◽  
pp. 1309-1313 ◽  
Author(s):  
R H Gooding ◽  
C M Challoner

Standard mapping procedures were used to map four loci in linkage group I (the X chromosome), two loci in linkage group II, and two loci in linkage group III of Glossina morsitans submorsitans. In the presence of the allele Srd (the distorter allele favoring production of female offspring), no recombination occurred between any of the following loci: Pgm (phosphoglucomutase), wht (white eye color), Est-X (a thoracic esterase), and Sr (sex-ratio distortion). However, in the absence of Srd (i.e., in females homozygous for Srn, the allele that permits males to sire both female and male offspring in approximately equal numbers), the loci Pgm and wht were separated by 23 ± 4.0% recombination (map distance). These results indicate that ourG. m. submorsitans strains carry two forms of the X chromosome, designated XA and XB. In support of this interpretation, two lines of G. m. submorsitans were established: in both lines, males with wild-type eyes sired families that were almost exclusively female, while males with white eyes sired families having males and females in approximately equal numbers. Two loci, Ao (aldehyde oxidase) and Est-1 (a thoracic esterase) were separated by 6.1 ± 2.3% recombination in linkage group II, and two loci, Mdh (malate dehydrogenase) and Pgi (phosphoglucose isomerase), showed 51.9 ± 4.9% recombination in linkage group III.


1968 ◽  
Vol 11 (2) ◽  
pp. 193-199 ◽  
Author(s):  
Mary F. Lyon ◽  
Jane M. Butler ◽  
Richard Kemp

In mice heterozygous for translocation T(2;?)163H, and also for linkage group II markers, the cw locus shows close linkage with the point of rearrangement (about 1−2% recombination). Since T 163 was apparently formed by fusion of two chromosomes near their centromeres, this means that the centromere must lie at the cw end of linkage group II. In homozygotes for T(2; 9)138Ca the genes T and d show significant linkage, indicating that their loci are on opposite sides of the trans-location break. Since, from previous data, the break is known to be proximal to d, it must then be distal to T and, again from previous data, the order of loci hi linkage group IX must be centromere-T-tf-T 138 break.


1981 ◽  
Vol 23 (3) ◽  
pp. 399-403 ◽  
Author(s):  
R. H. Gooding

Linkage group I is defined as the loci on the differential part of the X-chromosome of adult Glossina morsitans morsitans Westwood. Three loci are known and their order on the X-chromosome has been demonstrated as ocra (body color), salmon (eye color), and Apk (arginine phosphokinase, E.C. 2.7.3.3) with 38 map units separating the first two loci and 32 to 41 separating the second two. This region of the X-chromosome does not contain the chromosomal inversion known to occur in the Handeni line of G. m. morsitans. Linkage group II is defined as the autosome carrying the locus Xo (xanthine oxidase, E.C. 1.2.3.2), and it is demonstrated to carry also the loci Ao (aldehyde oxidase, E.C. 1.2.3.1) and Odh (octanol dehydrogenase, E.C. 1.1.1.73). Ao and Odh are within 0.36 map units of each other and have not been separated by recombination; this pair of loci occur about 48 map units from Xo. During mapping experiments, no evidence for genetical recombination was found in male G. m. morsitans.


Genetics ◽  
1978 ◽  
Vol 88 (1) ◽  
pp. 49-65
Author(s):  
Robert K Herman

ABSTRACT Two dominant suppressors of crossing over have been identified following X-ray treatment of the small nematode C. elegans. They suppress crossing over in linkage group II (LGII) about 100-fold and 50-fold and are both tightly linked to LGII markers. One, called C1, segregates independently of all other linkage groups and is homozygous fertile. The other is a translocation involving LGII and X. The translocation also suppresses rrossing over along the right half of X and is homozygous lethal. CI has been used as a balancer of LGII recessive lethal and sterile mutations induced by EMS. The frequencies of occurrence of lethals and steriles were approximately equal. Fourteen mutations were assigned to complementation groups and mapped. They tended to map in the same region where LGII visibles are clustered.


Genetics ◽  
1988 ◽  
Vol 119 (2) ◽  
pp. 355-363
Author(s):  
L A Jacobson ◽  
L Jen-Jacobson ◽  
J M Hawdon ◽  
G P Owens ◽  
M A Bolanowski ◽  
...  

Abstract Mutants of Caenorhabditis elegans having about 10% of wild-type activity of the aspartyl protease cathepsin D have been isolated by screening. Mutant homozygotes have normal growth rates and no obvious morphological or developmental abnormalities. The mutant gene (cad-1) has been mapped to the right extremity of linkage group II. Heterozygous animals (cad-1/+) show intermediate enzyme levels and animals heterozygous for chromosomal deficiencies of the right extremity of linkage group II have 50% of wild-type activity. Cathepsin D purified from a mutant strain has a lower activity per unit mass of pure enzyme. These data suggest that cad-1 is a structural gene for cathepsin D.


1986 ◽  
Vol 28 (4) ◽  
pp. 545-553 ◽  
Author(s):  
D. W. Nelson ◽  
B. M. Honda

We have identified a restriction fragment length difference (RFLD) affecting the genomic sequences immediately flanking the 5S rRNA gene cluster in the Bristol and Bergerac strains of the nematode Caenorhabditis elegans. We have used this RFLD as a molecular marker to follow the segregation of the 5S rRNA gene cluster through a series of two- and three-factor interstrain crosses. Our results show that the 5S rRNA gene cluster maps between unc-76 and dpy-21 on the right arm of linkage group V. This genetic localization provides a linkage group V "landmark" with which to localize other cloned sequences by in situ hybridization.Key words: Caenorhabditis elegans, 5S rRNA gene cluster, restriction fragment length difference, genetic mapping.


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.


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