RADIATION-SENSITIVE MUTANTS OF CAENORHABDITIS ELEGANS

Genetics ◽  
1982 ◽  
Vol 102 (2) ◽  
pp. 159-178
Author(s):  
Philip S Hartman ◽  
Robert K Herman
Keyword(s):  
Caenorhabditis Elegans ◽  
X Chromosome ◽  
Spontaneous Mutation ◽  
Radiation Sensitivity ◽  
Temperature Sensitive ◽  
X Rays ◽  
C Elegans ◽  
Elevated Frequency ◽  
Rad Mutants ◽  
Chromosome Nondisjunction

ABSTRACT Nine rad (for abnormal radiation sensitivity) mutants hypersensitive to ultraviolet light were isolated in the small nematode Caenorhabditis elegans. The mutations are recessive to their wild-type alleles, map to four of the six linkage groups in C. elegans and define nine new games named rad-1 through rad-9. Two of the mutants—rad-1 and rad-2—are very hypersensitive to X rays, and three—rad-2, rad-3 and rad-4—are hypersensitive to methyl methanesulfonate under particular conditions of exposure. The hypersensitivity of these mutants to more than one DNA-damaging agent suggests that they may be abnormal in DNA repair. One mutant—rad-5, a temperature-sensitive sterile mutant—shows an elevated frequency of spontaneous mutation at more than one locus; rad-4, which shows a cold-sensitive embryogenesis, reduces meiotic X-chromosome nondisjunction tenfold and partially suppresses some but not all mutations that increase meiotic X-chromosome nondisjunction; the viability of rad-6 hermaphrodites is half that of rad-6 males at 25°; and newly mature (but not older) rad-8 hermaphrodites produce many inviable embryo progeny. Meiotic recombination frequencies were measured for seven rad mutants and found to be close to normal.

scholarly journals Natural variations in reproductive aging phenotypes reveal the importance of early reproductive period in Caenorhabditis elegans

2021 ◽  
Author(s):  
Jiseon Lim ◽  
Jun Kim ◽  
Junho Lee
Keyword(s):  
Caenorhabditis Elegans ◽  
X Chromosome ◽  
Brood Size ◽  
Current Knowledge ◽  
Reproductive Capacity ◽  
Initial Population ◽  
Reproductive Aging ◽  
C Elegans ◽  
Wild Strains ◽  
Chromosome Nondisjunction

Although reproductive capacity is a major factor in individual fitness, aging of the reproductive system precedes somatic aging and may reduce the total brood size. Genetic studies have led to the development of a body of evolutionary theory in the nematode Caenorhabditis elegans, but these studies did not take into account current knowledge about the natural history of C. elegans. To enhance our understanding of reproductive aging in C. elegans, we measured and compared two reproductive aging-related traitsthe number of progeny and the X-chromosome nondisjunction rateof 96 wild strains during early, late and total reproductive periods. We found that the two traits exhibited natural phenotypic variation, with few outliers, and that the brood size and the X-chromosome nondisjunction rate were not genetically correlated. Contrary to a previous hypothesis, that reproductive aging contributes to the generation of an optimal total number of offspring, we found that the total brood size did not converge to an optimal value, and early brood size was more constant than total brood size among wild strains. We speculate that reproductive aging is a by-product of a rapid increase in the initial population size, which might be related to the boom-and-bust lifestyle of C. elegans. We also identified loci and candidate genetic variants significantly associated with X-chromosome nondisjunction rate in the late and total reproductive periods. Our results provide an insight into reproductive aging in wild C. elegans strains.

scholarly journals Natural variation in reproductive timing and X-chromosome nondisjunction in Caenorhabditis elegans

2021 ◽  
Author(s):  
Jiseon Lim ◽  
Jun Kim ◽  
Junho Lee
Keyword(s):  
Caenorhabditis Elegans ◽  
X Chromosome ◽  
Reproductive Timing ◽  
Male Production ◽  
C Elegans ◽  
In The Wild ◽  
Wild Strains ◽  
Large Brood ◽  
Insight Into ◽  
Chromosome Nondisjunction

Abstract Caenorhabditis elegans hermaphrodites first produce a limited number of sperm cells, before their germline switches to oogenesis. Production of progeny then ensues until sperm is depleted. Male production in the self-progeny of hermaphrodites occurs following X-chromosome nondisjunction during gametogenesis, and in the reference strain increases with age of the hermaphrodite parent. To enhance our understanding of the reproductive timecourse in C. elegans, we measured and compared progeny production and male proportion during the early and late reproductive periods of hermaphrodites for 96 wild C. elegans strains. We found that the two traits exhibited natural phenotypic variation with few outliers and a similar reproductive timing pattern as previous reports. Progeny number and male proportion were not correlated in the wild strains, implying that wild strains with a large brood size did not produce males at a higher rate. We also identified loci and candidate genetic variants significantly associated with male-production rate in the late and total reproductive periods. Our results provide an insight into life-history traits in wild C. elegans strains.

scholarly journals FHOD-1 is the only formin in Caenorhabditis elegans that promotes striated muscle growth and Z-line organization in a cell autonomous manner

2020 ◽  
Author(s):  
Sumana Sundaramurthy ◽  
SarahBeth Votra ◽  
Arianna Laszlo ◽  
Tim Davies ◽  
David Pruyne
Keyword(s):  
Caenorhabditis Elegans ◽  
Muscle Cell ◽  
Muscle Development ◽  
Striated Muscle ◽  
Muscle Growth ◽  
Temperature Sensitive ◽  
Direct Role ◽  
C Elegans ◽  
Simple Model System ◽  
Body Wall Muscles

AbstractThe striated body wall muscles of Caenorhabditis elegans are a simple model system with well-characterized sarcomeres that have many vertebrate protein homologs. Previously, we observed deletion mutants for two formin genes, fhod-1 and cyk-1, developed thin muscles with abnormal dense bodies/sarcomere Z-lines. However, the nature of the cyk-1 mutation necessitated maternal CYK-1 expression for viability of the examined animals. Here, we tested the effects of complete loss of CYK-1 using a fast acting temperature-sensitive cyk-1(ts) mutant. Surprisingly, neither post-embryonic loss of CYK-1 nor acute loss of CYK-1 during embryonic sarcomerogenesis caused muscle defects, suggesting CYK-1 might not play a direct role in muscle development. Consistent with this, examination of cyk-1(Δ) mutants re-expressing CYK-1 in a mosaic pattern showed CYK-1 cannot rescue muscle defects in a muscle cell autonomous manner, suggesting muscle phenotypes caused by cyk-1 deletion are likely indirect. Conversely, mosaic re-expression of FHOD-1 in fhod-1(Δ) mutants promoted muscle cell growth, as well as proper Z-line organization, in a muscle cell autonomous manner. As we can observe no effect of loss of any other worm formin on muscle development, we conclude that FHOD-1 is the only formin that directly promotes striated muscle development in C. elegans.

scholarly journals THE EFFECT OF TEMPERATURE AND PARENTAL AGE ON RECOMBINATION AND NONDISJUNCTION IN CAENORHABDITIS ELEGANS

Genetics ◽  
1979 ◽  
Vol 92 (2) ◽  
pp. 409-418 ◽  
Author(s):  
A M Rose ◽  
D L Baillie
Keyword(s):  
Recombination Event ◽  
Egg Production ◽  
Recombination Frequency ◽  
Temperature Shift ◽  
Effect Of Temperature ◽  
Temperature Sensitive ◽  
Parental Age ◽  
Linkage Groups ◽  
C Elegans ◽  
Chromosome Nondisjunction

ABSTRACT The effect of temperature and parental age on recombination frequency in C. elegans was studied between pairs of closely linked markers on linkage groups I and V. In the regions studied, recombination frequency vaned three-fold over the temperature range 13.5° to 26°. Temperature-shift experiments indicated that a temperature-sensitive recombination event occurs approximately 50 oocytes prior to fertilization. Recombination frequency was observed to decrease with maternal age. The greatest decrease was observed in the first 24 hours of egg production. The frequency of male progeny, a measure of X-chromosome nondisjunction was also studied. This frequency increased with elevated temperature and age of the parent.

scholarly journals Meiotic mutants that cause a polar decrease in recombination on the X chromosome in Caenorhabditis elegans.

Genetics ◽  
1994 ◽  
Vol 136 (1) ◽  
pp. 119-127
Author(s):  
S A Broverman ◽  
P M Meneely
Keyword(s):  
Caenorhabditis Elegans ◽  
Genetic Map ◽  
X Chromosome ◽  
Recessive Mutations ◽  
Feature Characteristic ◽  
Comparable Effect ◽  
Chromosome Recombination ◽  
The Right ◽  
Chromosome Nondisjunction ◽  
Pairing Region

Abstract Recessive mutations in three autosomal genes, him-1, him-5 and him-8, cause high levels of X chromosome nondisjunction in hermaphrodites of Caenorhabditis elegans, with no comparable effect on autosomal disjunction. Each of the mutants has reduced levels of X chromosome recombination, correlating with the increase in nondisjunction. However, normal or elevated levels of recombination occur at the end of the X chromosome hypothesized to contain the pairing region (the left end), with recombination levels decreasing in regions approaching the right end. Thus, both the number and the distribution of X chromosome exchange events are altered in these mutants. As a result, the genetic map of the X chromosome in the him mutants exhibits a clustering of genes due to reduced recombination, a feature characteristic of the genetic map of the autosomes in non-mutant animals. We hypothesize that these him genes are needed for some processive event that initiates near the left end of the X chromosome.

scholarly journals Rec-8 dimorphism affects longevity, stress resistance and X-chromosome nondisjunction in C. elegans, and replicative lifespan in S. cerevisiae

2014 ◽  
Vol 5 ◽  
Author(s):  
Srinivas Ayyadevara ◽  
Çagdas Tazearslan ◽  
Ramani Alla ◽  
James C. Jiang ◽  
S. Michal Jazwinski ◽  
...  
Keyword(s):  
X Chromosome ◽  
Stress Resistance ◽  
Replicative Lifespan ◽  
C Elegans ◽  
Chromosome Nondisjunction

scholarly journals LETHALS, STERILES AND DEFICIENCIES IN A REGION OF THE X CHROMOSOME OF CAENORHABDITIS ELEGANS

Genetics ◽  
1979 ◽  
Vol 92 (1) ◽  
pp. 99-115 ◽  
Author(s):  
Philip M Meneely ◽  
Robert K Herman
Keyword(s):  
Caenorhabditis Elegans ◽  
X Chromosome ◽  
Maternal Effect ◽  
Mutant Allele ◽  
Temperature Sensitive ◽  
Wild Type ◽  
Nematode Caenorhabditis Elegans ◽  
X Chromosomes ◽  
X Ray ◽  
Chromosome Duplication

ABSTRACT Twenty-one X-linked recessive lethal and sterile mutations balanced by an unlinked X-chromosome duplication have been identified following EMS treatment of the small nematode, Caenorhabditis elegans. The mutations have been assigned by complementation analysis to 14 genes, four of which have more than one mutant allele. Four mutants, all alleles, are temperature-sensitive embryonic lethals. Twelve mutants, in ten genes, are early larval lethals. TWO mutants are late larval lethals, and the expression of one of these is influenced by the number of X chromosomes in the genotype. Two mutants are maternal-effect lethals; for both, oocytes made by mutant hermaphrodites are rescuable by wild-type sperm. One of the maternal-effect lethals and two larval lethals are allelic. One mutant makes defective sperm. The lethals and steriles have been mapped by recombination and by complementation testing against 19 deficiencies identified after X-ray treatment. The deficiencies divide the region, about 15% of the X-chromosome linkage map, into at least nine segments. The deficiencies have also been used to check the phenotypes of hemizygous lethal and sterile hermaphrodites.

scholarly journals The dpy-30 gene encodes an essential component of the Caenorhabditis elegans dosage compensation machinery.

Genetics ◽  
1994 ◽  
Vol 137 (4) ◽  
pp. 999-1018 ◽  
Author(s):  
D R Hsu ◽  
B J Meyer
Keyword(s):  
Caenorhabditis Elegans ◽  
Sex Determination ◽  
X Chromosome ◽  
Dosage Compensation ◽  
The Other ◽  
Temperature Sensitive ◽  
Wild Type ◽  
Phenotypic Analysis ◽  
General Role ◽  
Essential Component

Abstract The need to regulate X chromosome expression in Caenorhabditis elegans arises as a consequence of the primary sex-determining signal, the X/A ratio (the ratio of X chromosomes to sets of autosomes), which directs 1X@A animals to develop as males and 2X/2A animals to develop as hermaphrodites. C. elegans possesses a dosage compensation mechanism that equalizes X chromosome expression between the two sexes despite their disparity in X chromosome dosage. Previous genetic analysis led to the identification of four autosomal genes, dpy-21, dpy-26, dpy-27 and dpy-28, whose products are essential in XX animals for proper dosage compensation, but not for sex determination. We report the identification and characterization of dpy-30, an essential component of the dosage compensation machinery. Putative null mutations in dpy-30 disrupt dosage compensation and cause a severe maternal-effect, XX-specific lethality. Rare survivors of the dpy-30 lethality are dumpy and express their X-linked genes at higher than wild-type levels. These dpy-30 mutant phenotypes superficially resemble those caused by mutations in dpy-26, dpy-27 and dpy-28; however, detailed phenotypic analysis reveals important differences that distinguish dpy-30 from these genes. In contrast to the XX-specific lethality caused by mutations in the other dpy genes, the XX-specific lethality caused by dpy-30 mutations is completely penetrant and temperature sensitive. In addition, unlike the other genes, dpy-30 is required for the normal development of XO animals. Although dpy-30 mutations do not significantly affect the viability of XO animals, they do cause them to be developmentally delayed and to possess numerous morphological and behavioral abnormalities. Finally, dpy-30 mutations can dramatically influence the choice of sexual fate in animals with an ambiguous sexual identity, despite having no apparent effect on the sexual phenotype of otherwise wild-type animals. Paradoxically, depending on the genetic background, dpy-30 mutations cause either masculinization or feminization, thus revealing the complex regulatory relationship between the sex determination and dosage compensation processes. The novel phenotypes caused by dpy-30 mutations suggest that in addition to acting in the dosage compensation process, dpy-30 may play a more general role in the development of both XX and XO animals.

scholarly journals Him-10 Is Required for Kinetochore Structure and Function on Caenorhabditis elegans Holocentric Chromosomes

2001 ◽  
Vol 153 (6) ◽  
pp. 1227-1238 ◽  
Author(s):  
Mary Howe ◽  
Kent L. McDonald ◽  
Donna G. Albertson ◽  
Barbara J. Meyer
Keyword(s):  
Caenorhabditis Elegans ◽  
Structure And Function ◽  
Holocentric Chromosomes ◽  
Molecular Architecture ◽  
Mitotic Chromosomes ◽  
C Elegans ◽  
Meiotic Chromosomes ◽  
Evolutionarily Conserved ◽  
And Function ◽  
Chromosome Nondisjunction

Macromolecular structures called kinetochores attach and move chromosomes within the spindle during chromosome segregation. Using electron microscopy, we identified a structure on the holocentric mitotic and meiotic chromosomes of Caenorhabditis elegans that resembles the mammalian kinetochore. This structure faces the poles on mitotic chromosomes but encircles meiotic chromosomes. Worm kinetochores require the evolutionarily conserved HIM-10 protein for their structure and function. HIM-10 localizes to the kinetochores and mediates attachment of chromosomes to the spindle. Depletion of HIM-10 disrupts kinetochore structure, causes a failure of bipolar spindle attachment, and results in chromosome nondisjunction. HIM-10 is related to the Nuf2 kinetochore proteins conserved from yeast to humans. Thus, the extended kinetochores characteristic of C. elegans holocentric chromosomes provide a guide to the structure, molecular architecture, and function of conventional kinetochores.

Conditional absence of mitosis-specific antigens in a temperature-sensitive embryonic-arrest mutant of Caenorhabditis elegans

1987 ◽  
Vol 87 (2) ◽  
pp. 305-314 ◽  
Author(s):  
R.M. Hecht ◽  
M. Berg-Zabelshansky ◽  
P.N. Rao ◽  
F.M. Davis
Keyword(s):  
Caenorhabditis Elegans ◽  
Mammalian Cells ◽  
Temperature Shift ◽  
Temperature Sensitive ◽  
Restrictive Temperature ◽  
C Elegans ◽  
Phosphatase Treatment ◽  
M Phase ◽  
A Cell ◽  
Embryonic Arrest

A monoclonal antibody, specific to phosphoproteins in mitotic HeLa cells was found to crossreact with a similar set of proteins in embryos of the nematode, Caenorhabditis elegans. In C. elegans, as in mammalian cells, the highly conserved antigenic epitope is associated with a family of high molecular weight polypeptides. The antigenic reactivity of these multiple proteins also depends on their phosphorylation, since antibody binding is reduced after alkaline phosphatase treatment. The antigens are detected at the centrosomes, and in the nuclear region and surrounding cytoplasm of mitotic cells. The significance of these antigens is emphasized by their absence at restrictive temperature in embryos of the temperature-sensitive embryonic-arrest mutant, emb-29V. Furthermore, temperature shift-down experiments suggest that the emb-29 mutation defines a cell division cycle function that affects an essential activity required for progression into M phase.

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