scholarly journals The generation and genetic analysis of suppressors of lethal mutations in the Caenorhabditis elegans rol-3(V) gene.

Genetics ◽  
1994 ◽  
Vol 136 (1) ◽  
pp. 129-143 ◽  
Author(s):  
W B Barbazuk ◽  
R C Johnsen ◽  
D L Baillie
Keyword(s):  
Caenorhabditis Elegans ◽  
Genetic Analysis ◽  
Genetic Interaction ◽  
Temperature Sensitive ◽  
Left Hand ◽  
Larval Stages ◽  
Allele Specific ◽  
Complementation Groups ◽  
Nematode Cuticle ◽  
Developmental Role

Abstract The Caenorhabditis elegans rol-3(e754) mutation is a member of a general class of mutations affecting gross morphology, presumably through disruption of the nematode cuticle. Adult worms homozygous for rol-3(e754) exhibit rotation about their long axis associated with a left-hand twisted cuticle, musculature, gut and ventral nerve cord. Our laboratory previously isolated 12 recessive lethal alleles of rol-3. All these lethal alleles cause an arrest in development at either early or mid-larval stages, suggesting that the rol-3 gene product performs an essential developmental function. Furthermore, through the use of the heterochronic mutants lin-14 and lin-29, we have established that the expression of rol-3(e754)'s adult specific visible function is not dependent on the presence of an adult cuticle. In an attempt to understand rol-3's developmental role we sought to identify other genes whose products interact with that of rol-3. Toward this end, we generated eight EMS induced and two gamma irradiation-induced recessive suppressors of the temperature sensitive (ts) mid-larval lethal phenotype of rol-3(s1040ts). These suppressors define two complementation groups srl-1 II and srl-2 III; and, while they suppress the rol-3(s1040) lethality, they do not suppress the adult specific visible rolling phenotype. Furthermore, there is a complex genetic interaction between srl-2 and srl-1 such that srl-2(s2506) fails to complement all srl alleles tested. These results suggest that srl-1 and srl-2 may share a common function and, thus, possibly constitute members of the same gene family. Mutations in both srl-1 and srl-2 produce no obvious hermaphrodite phenotypes in the absence of rol-3(s1040ts); however, males homozygous for either srl-1 or srl-2 display aberrant tail morphology. We present evidence suggesting that the members of srl-2 are not allele specific with respect to their suppression of rol-3 lethality, and that rol-3 may act in some way to influence proper posterior morphogenesis. Finally, based on our genetic analysis of rol-3 and the srl mutations, we present a model whereby the wild-type products of the srl loci act in a concerted manner to negatively regulate the rol-3 gene.

scholarly journals THE SELECTION OF S. CEREVISIAE MUTANTS DEFECTIVE IN THE START EVENT OF CELL DIVISION

Genetics ◽  
1980 ◽  
Vol 95 (3) ◽  
pp. 561-577 ◽  
Author(s):  
Steven I Reed
Keyword(s):  
Cell Division ◽  
Genetic Analysis ◽  
Linkage Map ◽  
Nuclear Genes ◽  
Temperature Sensitive ◽  
Restrictive Temperature ◽  
Mating Pheromone ◽  
Preliminary Characterization ◽  
Complementation Groups ◽  
Selection Of

ABSTRACT Thirty-three temperature-sensitive mutations defective in the start event of the cell division cycle of Saccharomyces cereuisiae were isolated and subjected to preliminary characterization. Complementation studies assigned these mutations to four complementation groups, one of which, cdc28, has been described previously. Genetic analysis revealed that these complementation groups define single nuclear genes, unlinked to one another. One of the three newly identified genes, cdc37, has been located in the yeast linkage map on chromosome IV, two meiotic map units distal to hom2.—Each mutation produces stage-specific arrest of cell division at start, the same point where mating pheromone interrupts division. After synchronization at start by incubation at the restrictive temperature, the mutants retain the capacity to enlarge and to conjugate.

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.

Genetic analysis of temperature-sensitive embryogenesis mutants in Caenorhabditis elegans

1981 ◽  
Vol 84 (1) ◽  
pp. 193-205 ◽  
Author(s):  
Randall Cassada ◽  
Edoardo Isnenghi ◽  
Marilyn Culotti ◽  
Gunter von Ehrenstein
Keyword(s):  
Caenorhabditis Elegans ◽  
Genetic Analysis ◽  
Temperature Sensitive

scholarly journals Genetic analysis of the adenosine3 (Gart) region of the second chromosome of Drosophila melanogaster.

Genetics ◽  
1990 ◽  
Vol 124 (4) ◽  
pp. 889-897
Author(s):  
S Y Tiong ◽  
D Nash
Keyword(s):  
Drosophila Melanogaster ◽  
Genetic Analysis ◽  
Gene Product ◽  
Genetic Interaction ◽  
Chromosome Region ◽  
The Other ◽  
Purine Biosynthesis ◽  
Induced Mutations ◽  
Complementation Groups ◽  
Functional Complexity

Abstract The Gart gene of Drosophila melanogaster is known, from molecular biological evidence, to encode a polypeptide that serves three enzymatic functions in purine biosynthesis. It is located in polytene chromosome region 27D. One mutation in the gene (ade3(1)) has been described previously. We report here forty new ethyl methanesulfonate-induced mutations selected aga!nst a synthetic deficiency of the region from 27C2-9 to ++28B3-4. The mutations were characterized cytogenetically and by complementation analysis. The analysis apparently identifies 12 simple complementation groups. In addition, two segments of the chromosome exhibit complex complementation behavior. The first, the 28A region, gave three recessive lethals and also contains three known visible mutants, spade (spd), Sternopleural (Sp) and wingless (wg); a complex pattern of genetic interaction in the region incorporates both the new and the previously known mutants. The second region is at 27D, where seven extreme semilethal mutations give a complex complementation pattern that also incorporates ade3(1). Since ade3(1) is defective in one of the enzymatic functions encoded in the Gart gene, we assume the other seven also affect the gene. The complexity of the complementation pattern presumably reflects the functional complexity of the gene product. The phenotypic effects of the mutants at 27D are very similar to those described for ade2 mutations, which also interrupt purine biosynthesis.

scholarly journals Suppressors of the organ-specific differentiation gene pha-1 of Caenorhabditis elegans.

Genetics ◽  
1991 ◽  
Vol 129 (1) ◽  
pp. 69-77 ◽  
Author(s):  
H Schnabel ◽  
G Bauer ◽  
R Schnabel
Keyword(s):  
Caenorhabditis Elegans ◽  
Temperature Sensitive ◽  
Lethal Gene ◽  
Wild Type ◽  
Nematode Caenorhabditis Elegans ◽  
X Ray ◽  
Organ Specific ◽  
Complementation Groups ◽  
Differentiation Gene ◽  
Two Temperature

Abstract The embryonic lethal gene pha-1 of the nematode Caenorhabditis elegans is required for late differentiation and morphogenesis of the pharynx in the developing embryo. Revertants of two temperature-sensitive alleles of pha-1 were isolated with the aim of obtaining mutations in genes that interact with pha-1. By various methods of mutagenesis, chemical, X-ray, transposon, or by spontaneous reversion, 220 recessive revertants were obtained, defining three complementation groups. The largest, sup-35 on linkage group (LG) III, maps close to but is separable from pha-1. This suppressor can exert its effect either maternally or zygotically to allow survival of pha-1(ts) embryos. The other two, sup-36 and sup-37, are required zygotically and map on LGIV and LGV, respectively. We have not noted a phenotype distinguishing any of the suppressors from wild type except for suppression of pha-1. That suppression is the null phenotype of at least sup-35 is indicated by the high frequency of mutation and by the fact that heterozygotes carrying sup-35 and a deficiency spanning the locus are also able to suppress. Five spontaneous mutations in sup-35 were found to be associated with recombination.

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 OSMOTIC AVOIDANCE DEFECTIVE MUTANTS OF THE NEMATODE CAENORHABDITIS ELEGANS

Genetics ◽  
1978 ◽  
Vol 90 (2) ◽  
pp. 243-256 ◽  
Author(s):  
Joseph G Culotti ◽  
Richard L Russell
Keyword(s):  
Caenorhabditis Elegans ◽  
Avoidance Behavior ◽  
Recessive Mutation ◽  
Temperature Sensitive ◽  
Wild Type ◽  
Nematode Caenorhabditis Elegans ◽  
Genetic Studies ◽  
Touch Sensitivity ◽  
Complementation Groups ◽  
High Concentrations

ABSTRACT A wild-type strain of the nematode Caenorhabditis elegans has been shown to avoid high concentrations of a number of sugars and salts. Individual and population assays for this response were developed and mutants were selected for their inability to avoid high concentrations of fructose or NaCl. Seven nonavoiding mutants representing six complementation groups were isolated and characterized. Genetic studies indicate that the mutants each carry a single recessive mutation responsible for the defective osmotic avoidance behavior. The map locations of the six complementation groups identified by these mutations have been determined. Mutants isolated for their inability to avoid fructose are also unable to avoid NaCl and vice versa. The mutants move normally, exhibit normal touch sensitivity, and, like wild type, follow isotherms in a radial thermal gradient. All of the mutants are at least partially defective in the attraction to sodium chloride exhibited by wild type. None of the mutants is temperature sensitive, and all exhibit defective osmotic avoidance behavior as young L1 larvae. Preliminary anatomical studies indicate selective sensory neuron changes in at least one mutant.

scholarly journals Suppressors of glp-1, a gene required for cell communication during development in Caenorhabditis elegans, define a set of interacting genes.

Genetics ◽  
1993 ◽  
Vol 135 (4) ◽  
pp. 1011-1022 ◽  
Author(s):  
E M Maine ◽  
J Kimble
Keyword(s):  
Caenorhabditis Elegans ◽  
Cell Fate ◽  
Cell Function ◽  
Germ Line ◽  
Control Cell ◽  
Cell Communication ◽  
Cell Interactions ◽  
Temperature Sensitive ◽  
Allele Specific ◽  
Mitotic Proliferation

Abstract The glp-1 gene is essential for two cell interactions that control cell fate in Caenorhabditis elegans: induction of anterior pharynx in the embryo and induction of mitotic proliferation in the germ line. To identify other genes involved in these cell interactions, we have isolated suppressors of two temperature sensitive alleles of glp-1. Each of 14 recessive suppressors rescues both embryonic and germline glp-1(ts) defects. These suppressors are extragenic and define a set of six genes designated sog, for suppressor of glp-1. Suppression of glp-1 is the only obvious phenotype associated with sog mutations. Mutations in different sog genes show allele-specific intergenic noncomplementation, suggesting that the sog gene products may interact. In addition, we have analyzed a semidominant mutation that suppresses only the glp-1 germline phenotype and has a conditional feminized phenotype of its own. None of the suppressors rescues a glp-1 null mutation and therefore they do not bypass a requirement for glp-1. Distal tip cell function remains necessary for germline proliferation in suppressed animals. These suppressor mutations identify genes that may encode other components of the glp-1 mediated cell-signaling pathway or regulate glp-1 expression.

scholarly journals The Dominant Temperature-Sensitive Lethal DTS7 of Drosophila melanogaster Encodes an Altered 20S Proteasome β-Type Subunit

Genetics ◽  
1999 ◽  
Vol 151 (1) ◽  
pp. 211-220 ◽  
Author(s):  
Kerrie A Smyth ◽  
John M Belote
Keyword(s):  
Missense Mutation ◽  
Genetic Interaction ◽  
Temperature Sensitive ◽  
20S Proteasome ◽  
Dependent Manner ◽  
Subunit Gene ◽  
Ambient Temperatures ◽  
Similar Phenotype ◽  
Allele Specific ◽  
Dominant Temperature Sensitive

Abstract Proteasomes are multicatalytic complexes that function as the major proteolytic machinery in regulated protein degradation. The eukaryotic 20S proteasome proteolytic core structure comprises 14 different subunits: 7 α-type and 7 β-type. DTS7 is a dominant temperature-sensitive (DTS) lethal mutation at 29° that also acts as a recessive lethal at ambient temperatures. DTS7 maps to cytological position 71AB. Molecular characterization of DTS7 reveals that this is caused by a missense mutation in a β-type subunit gene, β2. A previously characterized DTS mutant, l(3)73Ai1, results from a missense mutation in another β-type subunit gene, β6. These two mutants share a very similar phenotype, show a strong allele-specific genetic interaction, and are rescued by the same extragenic suppressor, Su(DTS)-1. We propose that these mutants might act as “poison subunits,” disrupting proteasome function in a dosage-dependent manner, and suggest how they may interact on the basis of the structure of the yeast 20S proteasome.

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