scholarly journals Pairing for recombination in LGV of Caenorhabditis elegans: a model based on recombination in deficiency heterozygotes.

Genetics ◽  
1990 ◽  
Vol 124 (3) ◽  
pp. 615-625
Author(s):  
R E Rosenbluth ◽  
R C Johnsen ◽  
D L Baillie
Keyword(s):  
Caenorhabditis Elegans ◽  
Linkage Group ◽  
Group V ◽  
Left Half ◽  
Model Based ◽  
The Right

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.

THE GENETIC ANALYSIS OF A RECIPROCAL TRANSLOCATION, eT1(III; V), IN CAENORHABDITIS ELEGANS

Genetics ◽  
1981 ◽  
Vol 99 (3-4) ◽  
pp. 415-428
Author(s):  
Raja E Rosenbluth ◽  
David L Baillie
Keyword(s):  
Caenorhabditis Elegans ◽  
Genetic Analysis ◽  
Gene Order ◽  
Reciprocal Translocation ◽  
New Order ◽  
Linkage Groups ◽  
Recombination Rates ◽  
Left Half ◽  
New Gene ◽  
The Right

ABSTRACT The Caenorhabditis elegans mutation e873, which results in a recessive uncoordinated phenotype (formerly named Unc-72) and which had been isolated after 32P t reatment (BRENNER1 974), has now been found to act as a crossover suppressor and to be associated with a translocation between linkage groups (LG's) IIIand V. The translocation has been named, eTl(ZI1; V); eT1acts as a dominant crossover suppressor for both the right half of LGIIIand the left half of LGV,providing a balancer for a total of 39 map units. The uncoordinated e873phenotype has been shown to be a consequence of Eminactive unr- 36111gene. It was possible to demonstrate that, in translocation heterozygotes, eT1chromosomes marked with either sma-3or dpy-11segregate from normal LGIII,while those marked with bli-5, sm-2or unc-42segregate from normal LGV.Since bli-5and sma-2are normally on LGIII,and dpy-11is normally on LGV,it is concluded that: (a) eT1is a reciprocal translocation; (b) there is a breakpoint between sma-3and sma-2in LGIII(the region containing unc- 36)and one between dpy-11and unc-42in LGV;(c) thera is no dominant centromere between sma-2and bli-5on LGIII,since in eT1these genes are not linked to a LGIIIcentromere. Similarly, it is highly unlikely that there is a centromere to the left of dpy-11on LGV.The new gene order in eT1was determined by measuring recombination rates between markers in eT1homozygotes. It is concluded that the new order is: dpy-1 sma-3 (break) dpy-11 unc-60,and bli-5 sma-2 (break) unc-42 unc-51.——Thisis the first analysis of a C. eleganstranslocation with respect to reciprocity, breakpoints and new gene order.

Analysis of lethal mutations induced in a mutator strain that activates transposable elements in Caenorhabditis elegans

Genome ◽  
1990 ◽  
Vol 33 (1) ◽  
pp. 109-114 ◽  
Author(s):  
Denise V. Clark ◽  
Robert C. Johnsen ◽  
Kim S. McKim ◽  
David L. Baillie
Keyword(s):  
Caenorhabditis Elegans ◽  
Linkage Group ◽  
Gamma Ray ◽  
Hot Spot ◽  
Single Gene ◽  
Gene Mutations ◽  
Group Iv ◽  
Group V ◽  
Mutator Strain ◽  
Lethal Mutations

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.

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
Keyword(s):  
Linkage Group ◽  
Neurospora Crassa ◽  
Group V ◽  
The Right

scholarly journals CROSSOVER SUPPRESSORS AND BALANCED RECESSIVE LETHALS IN CAENORHABDITIS ELEGANS

Genetics ◽  
1978 ◽  
Vol 88 (1) ◽  
pp. 49-65
Author(s):  
Robert K Herman
Keyword(s):  
Caenorhabditis Elegans ◽  
Linkage Group ◽  
The Other ◽  
Crossing Over ◽  
Linkage Groups ◽  
Recessive Lethal ◽  
X Ray ◽  
C Elegans ◽  
Complementation Groups ◽  
The Right

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.

scholarly journals Identification of a putative structural gene for cathepsin D in Caenorhabditis elegans.

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 ◽  
...  
Keyword(s):  
Caenorhabditis Elegans ◽  
Linkage Group ◽  
Structural Gene ◽  
Cathepsin D ◽  
Normal Growth ◽  
Mutant Gene ◽  
Wild Type ◽  
Type Activity ◽  
Group Ii ◽  
The Right

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.

Genetic mapping of the 5S rRNA gene cluster of the nematode Caenorhabditis elegans

1986 ◽  
Vol 28 (4) ◽  
pp. 545-553 ◽  
Author(s):  
D. W. Nelson ◽  
B. M. Honda
Keyword(s):  
Caenorhabditis Elegans ◽  
Linkage Group ◽  
Gene Cluster ◽  
5S Rrna ◽  
Rrna Gene ◽  
Nematode Caenorhabditis Elegans ◽  
Group V ◽  
Length Difference ◽  
5S Rrna Gene ◽  
Restriction Fragment Length

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.

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
Keyword(s):  
Caenorhabditis Elegans ◽  
Linkage Group ◽  
X Chromosome ◽  
Linkage Groups ◽  
Group V ◽  
Chromosome Map ◽  
Mitotic Instability ◽  
X Irradiation ◽  
Group Ii ◽  
Map Data

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.

scholarly journals Genomic organization in Caenorhabditis elegans: deficiency mapping on linkage group V(left)

1988 ◽  
Vol 52 (2) ◽  
pp. 105-118 ◽  
Author(s):  
Raja E. Rosenbluth ◽  
Teresa M. Rogalski ◽  
Robert C. Johnsen ◽  
Linda M. Addison ◽  
David L. Baillie
Keyword(s):  
Caenorhabditis Elegans ◽  
Linkage Group ◽  
Mutant Allele ◽  
Genomic Organization ◽  
Group V ◽  
Recessive Lethal ◽  
C Elegans ◽  
Lethal Mutations ◽  
Autosomal Region ◽  
Complementation Groups

SummaryIn this study we genetically analyse a large autosomal region (23 map units) in Caenorhabditis elegans. The region comprises the left half of linkage group V [LGV(left)] and is recombinationally balanced by the translocation eT1(III; V). We have used rearrangement breakpoints to subdivide the region from the left end of LGV to daf-11 into a set of 23 major zones. Twenty of these zones are balanced by eT1. To establish the zones we examined a total of 110 recessive lethal mutations derived from a variety of screening protocols. The mutations identified 12 deficiencies, 1 duplication, as well as 98 mutations that fell into 59 complementation groups, significantly increasing the number of available genetic sites on LGV. Twenty-six of the latter had more than 1 mutant allele. Significant differences were observed among the alleles of only 6 genes, 3 of which have at least one ‘visible’ allele. Several deficiencies and 3 alleles of let-336 were demonstrated to affect recombination. The duplication identified in this study is sDp30(V;X). Lethal mutations covered by sDp30 were not suppressed uniformly in hermaphrodites. The basis for this non-uniformity may be related to the mechanism of X chromosome dosage compensation in C. elegans.

Maternal-effect lethal mutations on linkage group II of Caenorhabditis elegans.

Genetics ◽  
1988 ◽  
Vol 120 (4) ◽  
pp. 977-986
Author(s):  
K J Kemphues ◽  
M Kusch ◽  
N Wolf
Keyword(s):  
Caenorhabditis Elegans ◽  
Linkage Group ◽  
Maternal Effect ◽  
Essential Genes ◽  
The Other ◽  
C Elegans ◽  
Lethal Mutations ◽  
Embryonic Lethal ◽  
Embryonic Lethal Mutations ◽  
F1 Progeny

Abstract We have analyzed a set of linkage group (LG) II maternal-effect lethal mutations in Caenorhabditis elegans isolated by a new screening procedure. Screens of 12,455 F1 progeny from mutagenized adults resulted in the recovery of 54 maternal-effect lethal mutations identifying 29 genes. Of the 54 mutations, 39 are strict maternal-effect mutations defining 17 genes. These 17 genes fall into two classes distinguished by frequency of mutation to strict maternal-effect lethality. The smaller class, comprised of four genes, mutated to strict maternal-effect lethality at a frequency close to 5 X 10(-4), a rate typical of essential genes in C. elegans. Two of these genes are expressed during oogenesis and required exclusively for embryogenesis (pure maternal genes), one appears to be required specifically for meiosis, and the fourth has a more complex pattern of expression. The other 13 genes were represented by only one or two strict maternal alleles each. Two of these are identical genes previously identified by nonmaternal embryonic lethal mutations. We interpret our results to mean that although many C. elegans genes can mutate to strict maternal-effect lethality, most genes mutate to that phenotype rarely. Pure maternal genes, however, are among a smaller class of genes that mutate to maternal-effect lethality at typical rates. If our interpretation is correct, we are near saturation for pure maternal genes in the region of LG II balanced by mnC1. We conclude that the number of pure maternal genes in C. elegans is small, being probably not much higher than 12.

scholarly journals COMPLEMENTATION ANALYSIS OF LINKED CIRCADIAN CLOCK MUTANTS OF NEUROSPORA CRASSA

Genetics ◽  
1976 ◽  
Vol 82 (1) ◽  
pp. 9-17 ◽  
Author(s):  
Jerry F Feldman ◽  
Marian N Hoyle
Keyword(s):  
Linkage Group ◽  
Circadian Clock ◽  
Neurospora Crassa ◽  
Period Length ◽  
Complementation Analysis ◽  
Wild Type ◽  
The Right

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.

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