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.

CAENORHABDITIS ELEGANS DEFICIENCY MAPPING

Genetics ◽  
1984 ◽  
Vol 108 (2) ◽  
pp. 331-345
Author(s):  
D Christine Sigurdson ◽  
Gail J Spanier ◽  
Robert K Herman
Keyword(s):  
Caenorhabditis Elegans ◽  
Linkage Group ◽  
Ethyl Methanesulfonate ◽  
Single Site ◽  
Crossing Over ◽  
Wild Type ◽  
Nematode Caenorhabditis Elegans ◽  
Recessive Lethal ◽  
X Ray ◽  
New Mutations

ABSTRACT Six schemes were used to identify 80 independent recessive lethal deficiencies of linkage group (LG) II following X-ray treatment of the nematode Caenorhabditis elegans. Complementation tests between the deficiencies and ethyl methanesulfonate-induced recessive visible, lethal and sterile mutations and between different deficiencies were used to characterize the extents of the deficiencies. Deficiency endpoints thus helped to order 36 sites within a region representing about half of the loci on LG II and extending over about 5 map units. New mutations occurring in this region can be assigned to particular segments of the map by complementation tests against a small number of deficiencies; this facilitates the assignment of single-site mutations to particular genes, as we illustrate. Five sperm-defective and five oocyte-defective LG II sterile mutants were identified and mapped. Certain deficiency-by-deficiency complementation tests allowed us to suggest that the phenotypes of null mutations at two loci represented by visible alleles are wild type and that null mutations at a third locus confer a visible phenotype. A segment of LG II that is about 12 map units long and largely devoid of identified loci seems to be greatly favored for crossing over.

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 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 The Caenorhabditis elegans rol-6 gene, which interacts with the sqt-1 collagen gene to determine organismal morphology, encodes a collagen.

1990 ◽  
Vol 10 (5) ◽  
pp. 2081-2089 ◽  
Author(s):  
J M Kramer ◽  
R P French ◽  
E C Park ◽  
J J Johnson
Keyword(s):  
Caenorhabditis Elegans ◽  
Restriction Site ◽  
Genetic Interaction ◽  
The Other ◽  
C Elegans ◽  
Allele Specific ◽  
Specific Restriction ◽  
The Right ◽  
Sequence Similarities ◽  
Dominant Suppressor

The rol-6 gene is one of the more than 40 loci in Caenorhabditis elegans that primarily affect organismal morphology. Certain mutations in the rol-6 gene produce animals that have the right roller phenotype, i.e., they are twisted into a right-handed helix. The rol-6 gene interacts with another gene that affects morphology, sqt-1; a left roller allele of sqt-1 acts as a dominant suppressor of a right roller allele of rol-6. The sqt-1 gene has previously been shown to encode a collagen. We isolated and sequenced the rol-6 gene and found that it also encodes a collagen. The rol-6 gene was identified by physical mapping of overlapping chromosomal deficiencies that cover the gene and by identification of an allele-specific restriction site alteration. The amino acid sequence of the collagen encoded by rol-6 is more similar to that of the sqt-1 collagen than to any of the other ten C. elegans cuticle collagen sequences compared. The locations of cysteine residues flanking the Gly-X-Y repeat regions of rol-6 and sqt-1 are identical, but differ from those in the other collagens. The sequence similarities between rol-6 and sqt-1 indicate that they represent a new collagen subfamily in C. elegans. These findings suggest that these two collagens physically interact, possibly explaining the genetic interaction seen between the rol-6 and sqt-1 genes.

A CROSSOVER SUPPRESSOR-ENHANCER SYSTEM IN THE MOSQUITO AEDES AEGYPTI

1971 ◽  
Vol 13 (3) ◽  
pp. 561-577 ◽  
Author(s):  
Satish C. Bhalla
Keyword(s):  
Linkage Group ◽  
Reciprocal Translocation ◽  
Paracentric Inversion ◽  
Chromosome 1 ◽  
Crossing Over ◽  
Linkage Groups ◽  
Group Iii ◽  
Partial Sterility ◽  
The Right ◽  
And Inversion

A small reciprocal translocation T(1;2)1 involving chromosomes 1 and 2 and a paracentric inversion In(1)3 on m chromosome (1) of A. aegypti interact to give peculiar but consistent crossover values. The system is termed COSES and is associated with partial sterility. In females it suppresses crossing over tremendously to the right of bz and enhances crossing over to its left. In the males it enhances crossing over to the right of m (only 3 crossover units away from bz) hut the region to its left remains unaffected. COSES also displays interchromosomal effects by enhancing crossing over in linkage group III. Cytological and genetic evidence for the presence of translocation and inversion are presented. All three pairs of chromosomes are correlated to the three linkage groups.

The Caenorhabditis elegans rol-6 gene, which interacts with the sqt-1 collagen gene to determine organismal morphology, encodes a collagen

1990 ◽  
Vol 10 (5) ◽  
pp. 2081-2089
Author(s):  
J M Kramer ◽  
R P French ◽  
E C Park ◽  
J J Johnson
Keyword(s):  
Caenorhabditis Elegans ◽  
Restriction Site ◽  
Genetic Interaction ◽  
The Other ◽  
C Elegans ◽  
Allele Specific ◽  
Specific Restriction ◽  
The Right ◽  
Sequence Similarities ◽  
Dominant Suppressor

The rol-6 gene is one of the more than 40 loci in Caenorhabditis elegans that primarily affect organismal morphology. Certain mutations in the rol-6 gene produce animals that have the right roller phenotype, i.e., they are twisted into a right-handed helix. The rol-6 gene interacts with another gene that affects morphology, sqt-1; a left roller allele of sqt-1 acts as a dominant suppressor of a right roller allele of rol-6. The sqt-1 gene has previously been shown to encode a collagen. We isolated and sequenced the rol-6 gene and found that it also encodes a collagen. The rol-6 gene was identified by physical mapping of overlapping chromosomal deficiencies that cover the gene and by identification of an allele-specific restriction site alteration. The amino acid sequence of the collagen encoded by rol-6 is more similar to that of the sqt-1 collagen than to any of the other ten C. elegans cuticle collagen sequences compared. The locations of cysteine residues flanking the Gly-X-Y repeat regions of rol-6 and sqt-1 are identical, but differ from those in the other collagens. The sequence similarities between rol-6 and sqt-1 indicate that they represent a new collagen subfamily in C. elegans. These findings suggest that these two collagens physically interact, possibly explaining the genetic interaction seen between the rol-6 and sqt-1 genes.

scholarly journals Two types of sites required for meiotic chromosome pairing in Caenorhabditis elegans.

Genetics ◽  
1993 ◽  
Vol 134 (3) ◽  
pp. 749-768 ◽  
Author(s):  
K S McKim ◽  
K Peters ◽  
A M Rose
Keyword(s):  
Caenorhabditis Elegans ◽  
Meiotic Chromosome ◽  
Chromosome Rearrangement ◽  
The Other ◽  
Crossing Over ◽  
Homologous Chromosomes ◽  
Associated Sequences ◽  
Suppressed Recombination ◽  
The Right ◽  
Chromosome I

Abstract Previous studies have shown that isolated portions of Caenorhabditis elegans chromosomes are not equally capable of meiotic exchange. These results led to the proposal that a homolog recognition region (HRR), defined as the region containing those sequences enabling homologous chromosomes to pair and recombine, is localized near one end of each chromosome. Using translocations and duplications we have localized the chromosome I HRR to the right end. Whereas the other half of chromosome I did not confer any ability for homologs to pair and recombine, deficiencies in this region dominantly suppressed recombination to the middle of the chromosome. These deletions may have disrupted pairing mechanisms that are secondary to and require an HRR. Thus, the processes of pairing and recombination appear to utilize at least two chromosomal elements, the HRR and other pairing sites. For example, terminal sequences from other chromosomes increase the ability of free duplications to recombine with their normal homologs, suggesting that telomere-associated sequences, homologous or nonhomologous, play a role in facilitating meiotic exchange. Recombination can also initiate at internal sites separated from the HRR by chromosome rearrangement, such as deletions of the unc-54 region of chromosome I. When crossing over was suppressed in a region of chromosome I, compensatory increases were observed in other regions. Thus, the presence of the HRR enabled recombination to occur but did not determine the distribution of the crossover events. It seems most likely that there are multiple initiation sites for recombination once homolog recognition has been achieved.

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.

The genetic and RFLP characterization of the left end of linkage group III in Caenorhabditis elegans

Genome ◽  
1993 ◽  
Vol 36 (4) ◽  
pp. 712-724 ◽  
Author(s):  
Dave Pilgrim
Keyword(s):  
Caenorhabditis Elegans ◽  
Linkage Group ◽  
Genetic Map ◽  
Physical Map ◽  
Group Iii ◽  
C Elegans ◽  
Genomic Regions ◽  
Caenorhabditis Elegans Genome ◽  
Selection Of

A genetic approach was taken to identify new transposable element Tc1 -dependent polymorphisms on the left end of linkage group III in the nematode Caenorhabditis elegans. The cloning of the genomic DNA surrounding the Tc1 allowed the selection of overlapping clones (from the collection being used to assemble the physical map of the C. elegans genome). A contig of approximately 600–800 kbp in the region has been identified, the genetic map of the region has been refined, and 10 new RFLPs as well as at least four previously characterized genetic loci have been positioned onto the physical map, to the resolution of a few cosmids. This analysis demonstrated the ability to combine physical and genetic mapping for the rapid analysis of large genomic regions (0.5–1 Mbp) in genetically amenable eukaryotes.Key words: Caenorhabditis elegans, genome analysis, RFLP, physical map, genetic map.

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