scholarly journals ESSENTIAL GENES AND DEFICIENCIES IN THE UNC-22 IV REGION OF CAENORHABDITIS ELEGANS

Genetics ◽  
1982 ◽  
Vol 102 (4) ◽  
pp. 725-736
Author(s):  
Teresa M Rogalski ◽  
Donald G Moerman ◽  
David L Baillie
Keyword(s):  
Caenorhabditis Elegans ◽  
Unit Interval ◽  
Essential Genes ◽  
The Other ◽  
Nematode Caenorhabditis Elegans ◽  
Muscle Structure ◽  
Lethal Mutations ◽  
Recombination Mapping ◽  
Wide Range ◽  
The Right

ABSTRACT Five formaldehyde-induced deficiencies that uncover unc-22 IV, a gene affecting muscle structure in the nematode Caenorhabditis elegans were isolated and positioned. The largest deficiency, sDf2, extends in both directions from unc-22 and is approximately 1.0-2.0 map units in length. The other four deficiencies, sDf7, sDf8, sDf9 and sDf10, are all smaller than sDf2 and are located within the region uncovered by this deficiency. Thirty-seven ethyl methanesulfonate-induced lethal and sterile mutations linked to unc-22 were isolated and tested for complementation with sDf2. Nineteen lethal mutations failed to complement sDf2. Sixteen of these were further positioned by recombination mapping and also by deficiency mapping with sDf7, sDf8, sDf9 and sDf10. These sixteen mutations define 11 new essential genes in this region. Eight of the genes lie in a 0.9-map unit interval to the left of unc-22, whereas the three remaining genes lie in a region of about 0.2 map units to the right of unc-22. We believe that two of the essential genes identified in this study, let-56 and let-52, are the adjacent genes on either side of unc-22. The lethal mutations exhibit a wide range of terminal phenotypes: from first stage larva to sterile adult.

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 organization of the unc-60 region in Caenorhabditis elegans.

Genetics ◽  
1988 ◽  
Vol 118 (1) ◽  
pp. 49-59
Author(s):  
K S McKim ◽  
M F Heschl ◽  
R E Rosenbluth ◽  
D L Baillie
Keyword(s):  
Caenorhabditis Elegans ◽  
Linkage Group ◽  
Gene Order ◽  
Chromosomal Region ◽  
Essential Genes ◽  
Ethyl Methanesulfonate ◽  
Induced Mutations ◽  
Nematode Caenorhabditis Elegans ◽  
Genetic Organization ◽  
Muscle Structure

Abstract We have investigated the chromosomal region around unc-60 V, a gene affecting muscle structure, in the nematode Caenorhabditis elegans. The region studied covers 3 map units and lies at the left end of linkage group (LG) V. Compared to the region around dpy-11 (at the center of LGV), the unc-60 region has relatively few visible genes per map unit. We found the same to be true for essential genes. By screening simultaneously for recessive lethals closely linked to either dpy-11 or unc-60, we recovered ethyl methanesulfonate-induced mutations in 10 essential genes near dpy-11 but in only two genes near unc-60. Four deficiency breakpoints were mapped to the unc-60 region. Using recombination and deficiency mapping we established the following gene order: let-336, unc-34, let-326, unc-60, emb-29, let-426. Regarding unc-60 itself, we compared the effect of ten alleles (including five isolated during this study) on hermaphrodite mobility and fecundity. We used intragenic mapping to position eight of these alleles. The results show that these alleles are not distributed uniformly within the gene, but map to two groups approximately 0.012 map unit apart.

The effects of translocations on recombination frequency in Caenorhabditis elegans.

Genetics ◽  
1988 ◽  
Vol 120 (4) ◽  
pp. 987-1001
Author(s):  
K S McKim ◽  
A M Howell ◽  
A M Rose
Keyword(s):  
Caenorhabditis Elegans ◽  
Dna Sequences ◽  
Meiotic Recombination ◽  
Recombination Frequency ◽  
Unit Interval ◽  
Nematode Caenorhabditis Elegans ◽  
Recombination Suppression ◽  
The Right ◽  
Chromosome I

Abstract In the nematode Caenorhabditis elegans, recombination suppression in translocation heterozygotes is severe and extensive. We have examined the meiotic properties of two translocations involving chromosome I, szT1(I;X) and hT1(I;V). No recombination was observed in either of these translocation heterozygotes along the left (let-362-unc-13) 17 map units of chromosome I. Using half-translocations as free duplications, we mapped the breakpoints of szT1 and hT1. The boundaries of crossover suppression coincided with the physical breakpoints. We propose that DNA sequences at the right end of chromosome I facilitate pairing and recombination. We use the data from translocations of other chromosomes to map the location of pairing sites on four other chromosomes. hT1 and szT1 differed markedly in their effect on recombination adjacent to the crossover suppressed region. hT1 had no effect on recombination in the adjacent interval. In contrast, the 0.8 map unit interval immediately adjacent to the szT1(I;X) breakpoint on chromosome I increased to 2.5 map units in translocation heterozygotes. This increase occurs in a chromosomal interval which can be expanded by treatment with radiation. These results are consistent with the suggestion that the szT1(I) breakpoint is in a region of DNA in which meiotic recombination is suppressed relative to the genomic average. We propose that DNA sequences disrupted by the szT1 translocation are responsible for determining the frequency of meiotic recombination in the vicinity of the breakpoint.

scholarly journals GENETIC ORGANIZATION OF THE REGION AROUND UNC-15 (I), A GENE AFFECTING PARAMYOSIN IN CAENORHABDITIS ELEGANS

Genetics ◽  
1980 ◽  
Vol 96 (3) ◽  
pp. 639-648 ◽  
Author(s):  
A M Rose ◽  
D L Baillie
Keyword(s):  
Fine Structure ◽  
Caenorhabditis Elegans ◽  
Muscle Protein ◽  
Average Distance ◽  
Unit Interval ◽  
Essential Genes ◽  
Induced Mutations ◽  
Nematode Caenorhabditis Elegans ◽  
Biochemical Studies ◽  
Complementation Groups

ABSTRACT In the nematode Caenorhabditis elegans mutants in the gene unc-15 (I) affect the muscle protein paramyosin (Waterston, Fishpool and Brenner 1977). We have characterized 20 ethyl methanesulfonate-induced mutations in essential genes closely linked to unc-15. These lethals defined 16 new complementation groups. In the 0.65 map-unit interval around unc-15 defined by dpy-14 and unc-56, seven newly identified genes have been mapped relative to five existing genes. At present, the average distance between genes in this region is approximately 0.05 map units. Two genes, unc-15 and unc-13, are only 0.025 map units apart. Partial fine-structure maps of alleles of these two genes have been constructed. This analysis of unc-15 and genes adjacent to it is the first in a series of genetic and biochemical studies directed towards understanding the control of unc-15 expression.

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.

Kosovo

2008 ◽  
Author(s):  
Tim Judah
Keyword(s):  
European Union ◽  
The Other ◽  
Self Determination ◽  
The European Union ◽  
Western Balkans ◽  
National Pride ◽  
Wide Range ◽  
The World ◽  
The Right ◽  
Accessible Format

On February 17, 2008, Kosovo declared its independence, becoming the seventh state to emerge from the break-up of the former Yugoslavia. A tiny country of just two million people, 90% of whom are ethnic Albanians, Kosovo is central - geographically, historically, and politically - to the future of the Western Balkans and, in turn, its potential future within the European Union. But the fate of both Kosovo, condemned by Serbian leaders as a “fake state” and the region as a whole, remains uncertain. In Kosovo: What Everyone Needs to Know, Tim Judah provides a straight-forward guide to the complicated place that is Kosovo. Judah, who has spent years covering the region, offers succinct, penetrating answers to a wide range of questions: Why is Kosovo important? Who are the Albanians? Who are the Serbs? Why is Kosovo so important to Serbs? What role does Kosovo play in the region and in the world? Judah reveals how things stand now and presents the history and geopolitical dynamics that have led to it. The most important of these is the question of the right to self-determination, invoked by the Kosovo Albanians, as opposed to right of territorial integrity invoked by the Serbs. For many Serbs, Kosovo's declaration of independence and subsequent recognition has been traumatic, a savage blow to national pride. Albanians, on the other hand, believe their independence rights an historical wrong: the Serbian conquest (Serbs say “liberation”) of Kosovo in 1912. For anyone wishing to understand both the history and possible future of Kosovo at this pivotal moment in its history, this book offers a wealth of insight and information in a uniquely accessible format.

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 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.

The fog-3 gene and regulation of cell fate in the germ line of Caenorhabditis elegans.

Genetics ◽  
1995 ◽  
Vol 139 (2) ◽  
pp. 561-577 ◽  
Author(s):  
R E Ellis ◽  
J Kimble
Keyword(s):  
Caenorhabditis Elegans ◽  
Germ Cell ◽  
Sexual Identity ◽  
Cell Fate ◽  
Germ Cells ◽  
Regulatory Network ◽  
Germ Line ◽  
The Other ◽  
Nematode Caenorhabditis Elegans ◽  
Inhibitory Interactions

Abstract In the nematode Caenorhabditis elegans, germ cells normally adopt one of three fates: mitosis, spermatogenesis or oogenesis. We have identified and characterized the gene fog-3, which is required for germ cells to differentiate as sperm rather than as oocytes. Analysis of double mutants suggests that fog-3 is absolutely required for spermatogenesis and acts at the end of the regulatory hierarchy controlling sex determination for the germ line. By contrast, mutations in fog-3 do not alter the sexual identity of other tissues. We also have characterized the null phenotype of fog-1, another gene required for spermatogenesis; we demonstrate that it too controls the sexual identity of germ cells but not of other tissues. Finally, we have studied the interaction of these two fog genes with gld-1, a gene required for germ cells to undergo oogenesis rather than mitosis. On the basis of these results, we propose that germ-cell fate might be controlled by a set of inhibitory interactions among genes that specify one of three fates: mitosis, spermatogenesis or oogenesis. Such a regulatory network would link the adoption of one germ-cell fate to the suppression of the other two.

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