scholarly journals A screen for nonconditional dauer-constitutive mutations in Caenorhabditis elegans.

Genetics ◽  
1994 ◽  
Vol 136 (3) ◽  
pp. 879-886 ◽  
Author(s):  
E A Malone ◽  
J H Thomas
Keyword(s):  
Caenorhabditis Elegans ◽  
Temperature Sensitive ◽  
Genetic Pathway ◽  
Parallel Pathways ◽  
Dauer Larva ◽  
Dauer Formation ◽  
New Gene ◽  
The One ◽  
And Function ◽  
New Mutations

Abstract In Caenorhabditis elegans, formation of the developmentally arrested dauer larva is induced by high levels of a constitutively secreted pheromone. Synergy between two groups of incompletely penetrant dauer-constitutive (Daf-c) mutations has recently led to a proposal that these two groups of genes are partially redundant and function in two parallel pathways that regulate dauer formation. A possible weakness in this reasoning is that the mutations used to identify the synergy were specifically obtained as incompletely penetrant mutations. Here we use screens to identify new Daf-c alleles without any requirement for partial penetrance. Nevertheless, 22 of the 25 new mutations are incompletely penetrant mutations in 6 previously identified genes. Among these are mutations in daf-8 and daf-19, genes for which only one mutation had been previously identified. Also included in this group are three daf-1 alleles that do not exhibit the maternal rescue characteristic of other daf-1 alleles. Two of the 25 new mutations are fully penetrant and are alleles of daf-2, the one gene in which a fully penetrant mutation had been found earlier. Finally, one of the 25 new mutations is semidominant, temperature-sensitive, and identifies a new gene, daf-28. The results demonstrate that an incompletely penetrant Daf-c phenotype is characteristic of mutations in most Daf-c genes other than daf-2. This finding strengthens the hypothesis that a branched genetic pathway controls dauer formation.

scholarly journals Mutations affecting the meiotic and mitotic divisions of the early Caenorhabditis elegans embryo.

Genetics ◽  
1990 ◽  
Vol 126 (3) ◽  
pp. 593-605 ◽  
Author(s):  
P E Mains ◽  
K J Kemphues ◽  
S A Sprunger ◽  
I A Sulston ◽  
W B Wood
Keyword(s):  
Caenorhabditis Elegans ◽  
Maternal Effect ◽  
Mutant Gene ◽  
Temperature Sensitive ◽  
Loss Of Function ◽  
Gain Of Function ◽  
Lethal Mutations ◽  
Cell Embryo ◽  
New Gene ◽  
The One

Abstract We describe interactions between maternal-effect lethal mutations in four genes of Caenorhabditis elegans whose products appear to be involved in the meiotic and mitotic divisions of the one-cell embryo. Mitosis is disrupted by two dominant temperature-sensitive gain-of-function maternal-effect lethal mutations, mei-1(ct46) and mel-26(ct61), and by recessive loss-of-function maternal-effect lethal mutations of zyg-9. The phenotypic defects resulting from these mutations are similar. Doubly mutant combinations show a strong enhancement of the maternal-effect lethality under semipermissive conditions, suggesting that the mutant gene products interact. We isolated 15 dominant suppressors of the gain-of-function mutation mei-1(ct46). Thirteen of these suppressors are apparently intragenic, but 11 of them suppress in trans as well as cis. Two extragenic suppressors define a new gene, mei-2. The suppressor mutations in these two genes also result in recessive maternal-effect lethality, but with meiotic rather than mitotic defects. Surprisingly, most of these suppressors are also able to suppress mel-26(ct61) in addition to mei-1(ct46). The products of the four genes mei-1, mei-2, zyg-9 and mel-26 could be responsible for some of the specialized features that distinguish the meiotic from the mitotic divisions in the one-cell embryo.

scholarly journals Two Pleiotropic Classes of daf-2 Mutation Affect Larval Arrest, Adult Behavior, Reproduction and Longevity in Caenorhabditis elegans

Genetics ◽  
1998 ◽  
Vol 150 (1) ◽  
pp. 129-155 ◽  
Author(s):  
David Gems ◽  
Amy J Sutton ◽  
Mark L Sundermeyer ◽  
Patrice S Albert ◽  
Kevin V King ◽  
...  
Keyword(s):  
Caenorhabditis Elegans ◽  
Adult Longevity ◽  
Temperature Sensitive ◽  
Adult Behavior ◽  
Dauer Larva ◽  
Class 1 ◽  
Low Levels ◽  
Dauer Larvae ◽  
Overlapping Classes ◽  
Receptor Family

Abstract The nematode Caenorhabditis elegans responds to overcrowding and scarcity of food by arresting development as a dauer larva, a nonfeeding, long-lived, stress-resistant, alternative third-larval stage. Previous work has shown that mutations in the genes daf-2 (encoding a member of the insulin receptor family) and age-1 (encoding a PI 3-kinase) result in constitutive formation of dauer larvae (Daf-c), increased adult longevity (Age), and increased intrinsic thermotolerance (Itt). Some daf-2 mutants have additional developmental, behavioral, and reproductive defects. We have characterized in detail 15 temperature-sensitive and 1 nonconditional daf-2 allele to investigate the extent of daf-2 mutant defects and to examine whether specific mutant traits correlate with each other. The greatest longevity seen in daf-2 mutant adults was approximately three times that of wild type. The temperature-sensitive daf-2 mutants fell into two overlapping classes, including eight class 1 mutants, which are Daf-c, Age, and Itt, and exhibit low levels of L1 arrest at 25.5°. Seven class 2 mutants also exhibit the class 1 defects as well as some or all of the following: reduced adult motility, abnormal adult body and gonad morphology, high levels of embryonic and L1 arrest, production of progeny late in life, and reduced brood size. The strengths of the Daf-c, Age, and Itt phenotypes largely correlated with each other but not with the strength of class 2-specific defects. This suggests that the DAF-2 receptor is bifunctional. Examination of the null phenotype revealed a maternally rescued egg, L1 lethal component, and a nonconditional Daf-c component. With respect to the Daf-c phenotype, the dauer-defective (Daf-d) mutation daf-12(m20) was epistatic to daf-2 class 1 alleles but not the severe class 2 alleles tested. All daf-2 mutant defects were suppressed by the daf-d mutation daf-16(m26). Our findings suggest a new model for daf-2, age-1, daf-12, and daf-16 interactions.

scholarly journals Genetic analysis of chemosensory control of dauer formation in Caenorhabditis elegans.

Genetics ◽  
1992 ◽  
Vol 130 (1) ◽  
pp. 105-123 ◽  
Author(s):  
J J Vowels ◽  
J H Thomas
Keyword(s):  
Caenorhabditis Elegans ◽  
Genetic Analysis ◽  
Single Step ◽  
Genetic Interactions ◽  
The Other ◽  
Environmental Cues ◽  
Dauer Larva ◽  
Chemosensory Transduction ◽  
Dauer Formation ◽  
Dauer Larvae

Abstract Dauer larva formation in Caenorhabditis elegans is controlled by chemosensory cells that respond to environmental cues. Genetic interactions among mutations in 23 genes that affect dauer larva formation were investigated. Mutations in seven genes that cause constitutive dauer formation, and mutations in 16 genes that either block dauer formation or result in the formation of abnormal dauers, were analyzed. Double mutants between dauer-constitutive and dauer-defective mutations were constructed and characterized for their capacity to form dauer larvae. Many of the genes could be interpreted to lie in a simple linear epistasis pathway. Three genes, daf-16, daf-18 and daf-20, may affect downstream steps in a branched part of the pathway. Three other genes, daf-2, daf-3 and daf-5, displayed partial or complex epistasis interactions that were difficult to interpret as part of a simple linear pathway. Dauer-defective mutations in nine genes cause structurally defective chemosensory cilia, thereby blocking chemosensation. Mutations in all nine of these genes appear to fall at a single step in the epistasis pathway. Dauer-constitutive mutations in one gene, daf-11, were strongly suppressed for dauer formation by mutations in the nine cilium-structure genes. Mutations in the other six dauer-constitutive genes caused dauer formation despite the absence of functional chemosensory endings. These results suggest that daf-11 is directly involved in chemosensory transduction essential for dauer formation, while the other Daf-c genes play roles downstream of the chemosensory step.

scholarly journals egl-4 Acts Through a Transforming Growth Factor-β/SMAD Pathway in Caenorhabditis elegans to Regulate Multiple Neuronal Circuits in Response to Sensory Cues

Genetics ◽  
2000 ◽  
Vol 156 (1) ◽  
pp. 123-141 ◽  
Author(s):  
Susan A Daniels ◽  
Michael Ailion ◽  
James H Thomas ◽  
Piali Sengupta
Keyword(s):  
Caenorhabditis Elegans ◽  
Transforming Growth Factor ◽  
Transforming Growth Factor Β ◽  
Egg Laying ◽  
Sensory Cues ◽  
C Elegans ◽  
Epistasis Analysis ◽  
Dauer Larva ◽  
Dauer Formation ◽  
Chemosensory Behavior

Abstract Sensory cues regulate several aspects of behavior and development in Caenorhabditis elegans, including entry into and exit from an alternative developmental stage called the dauer larva. Three parallel pathways, including a TGF-β-like pathway, regulate dauer formation. The mechanisms by which the activities of these pathways are regulated by sensory signals are largely unknown. The gene egl-4 was initially identified based on its egg-laying defects. We show here that egl-4 has many pleiotropies, including defects in chemosensory behavior, body size, synaptic transmission, and dauer formation. Our results are consistent with a role for egl-4 in relaying sensory cues to multiple behavioral and developmental circuits in C. elegans. By epistasis analysis, we also place egl-4 in the TGF-β-like branch and show that a SMAD gene functions downstream of egl-4 in multiple egl-4-regulated pathways, including chemosensation.

scholarly journals Positive Selection of Caenorhabditis elegans Mutants With Increased Stress Resistance and Longevity

Genetics ◽  
2003 ◽  
Vol 163 (1) ◽  
pp. 171-180 ◽  
Author(s):  
Manuel J Muñoz ◽  
Donald L Riddle
Keyword(s):  
Thermal Stress ◽  
Caenorhabditis Elegans ◽  
Stress Resistance ◽  
Temperature Sensitive ◽  
Nematode Caenorhabditis Elegans ◽  
New Genes ◽  
Dauer Formation ◽  
F2 Progeny ◽  
New Alleles ◽  
Selection Of

Abstract We developed selective conditions for long-lived mutants of the nematode Caenorhabditis elegans by subjecting the first larval stage (L1) to thermal stress at 30° for 7 days. The surviving larvae developed to fertile adults after the temperature was shifted to 15°. A total of one million F2 progeny and a half million F3 progeny of ethyl-methanesulfonate-mutagenized animals were treated in three separate experiments. Among the 81 putative mutants that recovered and matured to the reproductive adult, 63 retested as thermotolerant and 49 (80%) exhibited a >15% increase in mean life span. All the known classes of dauer formation (Daf) mutant that affect longevity were found, including six new alleles of daf-2, and a unique temperature-sensitive, dauer-constitutive allele of age-1. Alleles of dyf-2 and unc-13 were isolated, and mutants of unc-18, a gene that interacts with unc-13, were also found to be long lived. Thirteen additional mutations define at least four new genes.

scholarly journals P2 Growth Restriction on an rpoC Mutant Is Suppressed by Alleles of the Rz1 Homolog lysC

2004 ◽  
Vol 186 (14) ◽  
pp. 4628-4637 ◽  
Author(s):  
Dmitry Markov ◽  
Gail E. Christie ◽  
Brian Sauer ◽  
Richard Calendar ◽  
Taehyun Park ◽  
...  
Keyword(s):  
Gene Arrangement ◽  
Growth Defect ◽  
Temperature Sensitive ◽  
Host Gene Expression ◽  
Accessory Gene ◽  
Reading Frame ◽  
Progeny Phage ◽  
Bacteriophage P2 ◽  
New Gene ◽  
And Function

ABSTRACT Escherichia coli strain 397c carries a temperature-sensitive mutation, rpoC397, that removes the last 50 amino acids of the RNA polymerase β′ subunit and is nonpermissive for plating of bacteriophage P2. P2 gor mutants productively infect 397c and define a new gene, lysC, encoded by a reading frame that extensively overlaps the P2 lysis accessory gene, lysB. The unusual location of lysC with respect to lysB is reminiscent of the Rz/Rz1 lysis gene pair of phage λ. Indeed, coexpression of lysB and lysC complemented the growth defect of λ Rz/Rz1 null mutants, indicating that the LysB/C pair is similar to Rz/Rz1 in both gene arrangement and function. Cells carrying the rpoC397 mutation exhibited an early onset of P2-induced lysis, which was suppressed by the gor mutation in lysC. We propose that changes in host gene expression resulting from the rpoC397 mutation result in changes in the composition of the bacterial cell wall, making the cell more susceptible to P2-mediated lysis and preventing accumulation of progeny phage sufficient for plaque formation.

scholarly journals A VISIBLE ALLELE OF THE MUSCLE GENE sup-10 X OF C. ELEGANS

Genetics ◽  
1986 ◽  
Vol 113 (1) ◽  
pp. 63-72
Author(s):  
Iva Greenwald ◽  
H Robert Horvitz
Keyword(s):  
Caenorhabditis Elegans ◽  
Protein Complex ◽  
Structure And Function ◽  
The Other ◽  
Wild Type ◽  
C Elegans ◽  
Muscle Structure ◽  
New Gene ◽  
Muscle Gene ◽  
And Function

ABSTRACT In this paper, we extend our previous analyses of a set of genes in Caenorhabditis elegans that are involved in muscle structure and function: unc-93 III, sup-9 II, sup-10 X and sup-11 I. We describe an unusual, visible allele of sup-10, examine how this allele interacts genetically with mutations in other genes of this set and propose that the wild-type products of the unc-93 and sup-10 loci may be components of a protein complex. We also describe a new gene of this set, sup-18 III, and the interaction of sup-18 alleles with mutations in the other genes.

scholarly journals Evidence for parallel processing of sensory information controlling dauer formation in Caenorhabditis elegans.

Genetics ◽  
1993 ◽  
Vol 134 (4) ◽  
pp. 1105-1117 ◽  
Author(s):  
J H Thomas ◽  
D A Birnby ◽  
J J Vowels
Keyword(s):  
Caenorhabditis Elegans ◽  
Parallel Processing ◽  
Sensory Information ◽  
Parallel Pathways ◽  
Dauer Formation ◽  
Group 2 ◽  
Group 1

Abstract Dauer formation in Caenorhabditis elegans is induced by chemosensation of high levels of a constitutively secreted pheromone. Seven genes defined by mutations that confer a dauer-formation constitutive phenotype (Daf-c) can be congruently divided into two groups by any of three criteria. Group 1 genes (daf-11 and daf-21) are (1) strongly synergistic with group 2 genes for their Daf-c phenotype, (2) incompletely suppressed by dauer-formation defective (Daf-d) mutations in the genes daf-3 and daf-5 and (3) strongly suppressed by Daf-d mutations in nine genes that affect the structure of chemosensory endings. Group 2 genes (daf-1, daf-4, daf-7, daf-8 and daf-14) are (1) strongly synergistic with group 1 genes for their Daf-c phenotype, (2) fully suppressed by Daf-d mutations in daf-3 and daf-5 and (3) not suppressed by Daf-d mutations in the nine genes that affect chemosensory ending structure. Mutations in each group of genes also cause distinct additional behavioral defects. We propose that these two groups of Daf-c genes act in parallel pathways that process sensory information. The two pathways are partially redundant with each other and normally act in concert to control dauer formation.

scholarly journals Genes that regulate both development and longevity in Caenorhabditis elegans.

Genetics ◽  
1995 ◽  
Vol 139 (4) ◽  
pp. 1567-1583 ◽  
Author(s):  
P L Larsen ◽  
P S Albert ◽  
D L Riddle
Keyword(s):  
Caenorhabditis Elegans ◽  
Life Span ◽  
Adult Life ◽  
Growth Conditions ◽  
Genetic Pathway ◽  
Adult Life Span ◽  
Dauer Larva ◽  
Separate Branch ◽  
Allele Specific ◽  
Limited Food

Abstract The nematode Caenorhabditis elegans responds to conditions of overcrowding and limited food by arresting development as a dauer larva. Genetic analysis of mutations that alter dauer larva formation (daf mutations) is presented along with an updated genetic pathway for dauer vs. nondauer development. Mutations in the daf-2 and daf-23 genes double adult life span, whereas mutations in four other dauer-constitutive genes positioned in a separate branch of this pathway (daf-1, daf-4, daf-7 and daf-8) do not. The increased life spans are suppressed completely by a daf-16 mutation and partially in a daf-2; daf-18 double mutant. A genetic pathway for determination of adult life span is presented based on the same strains and growth conditions used to characterize Daf phenotypes. Both dauer larva formation and adult life span are affected in daf-2; daf-12 double mutants in an allele-specific manner. Mutations in daf-12 do not extend adult life span, but certain combinations of daf-2 and daf-12 mutant alleles nearly quadruple it. This synergistic effect, which does not equivalently extend the fertile period, is the largest genetic extension of life span yet observed in a metazoan.

Sign in / Sign up

Export Citation Format

Share Document