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.

scholarly journals The unc-22(IV) region of Caenorhabditis elegans: genetic analysis of lethal mutations.

Genetics ◽  
1988 ◽  
Vol 119 (2) ◽  
pp. 345-353
Author(s):  
D V Clark ◽  
T M Rogalski ◽  
L M Donati ◽  
D L Baillie
Keyword(s):  
Caenorhabditis Elegans ◽  
Linkage Group ◽  
Essential Gene ◽  
Group Iv ◽  
Essential Genes ◽  
Ems Mutagenesis ◽  
Lethal Mutations ◽  
Complementation Groups ◽  
Minimum Estimate ◽  
Caenorhabditis Elegans Genome

Abstract The organization of essential genes in the unc-22 region, defined by the deficiency sDf2 on linkage group IV, has been studied. Using the balancer nT1 (IV;V), which suppresses recombination over 49 map units, 294 lethal mutations on LGIV(right) and LGV(left) were recovered using EMS mutagenesis. Twenty-six of these mutations fell into the unc-22 region. Together with previously isolated lethal mutations, there is now a total of 63 lethal mutations which fall into 31 complementation groups. Mutations were positioned on the map using eight overlapping deficiencies in addition to sDf2. The lethal alleles and deficiencies in the unc-22 region were characterized with respect to their terminal phenotypes. Mapping of these lethal mutations shows that sDf2 deletes a minimum of 1.8 map units and a maximum of 2.5 map units. A minimum estimate of essential gene number for the region using a truncated Poisson calculation is 48. The data indicate a minimum estimate of approximately 3500 essential genes in the Caenorhabditis elegans genome.

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.

scholarly journals Genetic analysis of a large autosomal region in Caenorhabditis elegans by the use of a free duplication

1987 ◽  
Vol 49 (3) ◽  
pp. 207-213 ◽  
Author(s):  
A. M. Howell ◽  
S. G. Gilmour ◽  
R. A. Mancebo ◽  
A. M. Rose
Keyword(s):  
Caenorhabditis Elegans ◽  
Gamma Radiation ◽  
Essential Gene ◽  
Single Gene ◽  
Gene Mutations ◽  
Essential Genes ◽  
Induced Mutations ◽  
Lethal Mutations ◽  
Autosomal Region ◽  
Complementation Groups

SummaryIn this paper we describe the use of a free duplication, sDp2 (I;f), for the recovery, maintenance, and analysis of mutations defining essential genes in the left third of Linkage Group I of Caenorhabditis elegans. The lethals were induced in a strain of genotype (sDp2) + /dpy-5 + unc-13/ dpy-5 unc-15 +, using either 12 mM ethylmethane sulphonate or 1500 r of gamma radiation. Lethal mutations linked to the dpy-5 unc-13 chromosome were recognized by the absence of Dpy-5 Unc-13 individuals amongst the self progeny and were maintained by isolating Unc-13 hermaphrodites. These strains – which have two mutant alleles of the essential gene and a wild-type allele on the duplication – are balanced, since crossing-over does not occur between sDp2 and the normal homologues. Using this sytem we have recovered 58 EMS-induced mutations. These have been characterized with regard to map position and complementation. Twenty-nine of the EMS-induced mutations lie to the left of dpy-5 and define 20 complementation groups; 3 were inseparable from dpy-5 and define 3 complementation groups; 21 were to the right and define 17 complementation groups. Among a set of 29 gamma radiation-induced lethal mutations, 17 appear to be single gene mutations or are very small deletions. We estimate that we have identified from one-sixth to one-half of the essential genes in the sDp2 region.

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 Genetic Analysis of Adult-Specific Surface Antigenic Differences Between Varieties of the Nematode Caenorhabditis elegans

Genetics ◽  
1987 ◽  
Vol 117 (3) ◽  
pp. 467-476
Author(s):  
Samuel M Politz ◽  
Karl J Chin ◽  
Daniel L Herman
Keyword(s):  
Caenorhabditis Elegans ◽  
Linkage Group ◽  
Genetic Analysis ◽  
Surface Antigen ◽  
Single Gene ◽  
Surface Antigens ◽  
Nematode Caenorhabditis Elegans ◽  
Specific Antibodies ◽  
C Elegans ◽  
Stage Specificity

ABSTRACT We have studied developmental stage-specificity and genetic specification of surface antigens in the nematode Caenorhabditis elegans. Rabbit antisera directed against the adult C. elegans cuticle were used in conjunction with antiserum adsorption experiments to obtain antibody reagents with specificity for the adult surface. Adult-specific antibodies were used to identify several varietal strains of C. elegans that display antigen-negative phenotypes as adults. Genetic mapping results using the surface antigen phenotype as a marker indicated that a single gene (designated srf-1) or cluster of genes on linkage group II determines the adult surface antigen phenotype.

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 CHROMOSOME REARRANGEMENTS IN CAENORHABDITIS ELEGANS

Genetics ◽  
1976 ◽  
Vol 83 (1) ◽  
pp. 91-105
Author(s):  
Robert K Herman ◽  
Donna G Albertson ◽  
Sydney Brenner
Keyword(s):  
Linkage Group ◽  
Fluorescence Microscopy ◽  
The Other ◽  
Crossing Over ◽  
Group V ◽  
X Chromosomes ◽  
Recessive Lethal ◽  
C Elegans ◽  
Lethal Mutations ◽  
Chromosome Fragments

ABSTRACT A method for selecting unlinked duplications of a part of the X chromosome of C. elegans is described. Five such duplications have been identified. One of them, Dp(X;V)1, is translocated to linkage group V, where it suppresses crossing over along the left half of linkage group V. Dp(X;V)1 homozygotes grow slowly and are sterile. The other four duplications are associated with chromosome fragments, as observed cytologically by fluorescence microscopy, and tend to be lost. Their frequency of loss is higher in strains homozygous for a mutation that promotes nondisjunction of X chromosomes. The recombination frequencies between two of these duplications and the X have been measured: the frequencies are at least 50 times less than for X-X recombination in the same region. The duplications may prove useful as balancers of recessive lethal mutations.

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 LINKAGE ANALYSIS OF NYSTATIN RESISTANCE MUTATIONS IN DICTYOSTELIUM DISCOIDEUM

Genetics ◽  
1986 ◽  
Vol 113 (1) ◽  
pp. 53-62
Author(s):  
Dennis L Welker
Keyword(s):  
Linkage Group ◽  
Linkage Analysis ◽  
Dictyostelium Discoideum ◽  
Group Iv ◽  
Resistance Locus ◽  
Resistance Mutations ◽  
Group Vi ◽  
Group V ◽  
The Third ◽  
Nystatin Resistance

ABSTRACT Earlier linkage analyses of nystatin resistance loci in Dictyostelium discoideum tentatively mapped the nysB and nysC loci to the previously unmarked linkage group V. The data presented here establishes that nysB maps to linkage group VI and that nysC maps to linkage group IV. The third nystatin resistance locus, nysA, maps to linkage group II.

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