A CYTOGENETICAL ANALYSIS OF STERILE MUTANTS IN CAENORHABDITIS ELEGANS

1980 ◽  
Vol 22 (3) ◽  
pp. 391-403 ◽  
Author(s):  
Nicole Mounier ◽  
Jean Brun
Keyword(s):  
Caenorhabditis Elegans ◽  
Oocyte Maturation ◽  
Chromosome Pairing ◽  
Male Meiosis ◽  
Cytological Analysis ◽  
Wild Type ◽  
Nematode Caenorhabditis Elegans ◽  
The Third ◽  
Homozygous Mutant ◽  
Cytogenetical Analysis

The regulation of gametogenesis in the hermaphrodite and proterandrous nematode Caenorhabditis elegans is introduced here through the analysis of nonconditional sterile mutants. To investigate the mechanisms which allow the two gametogenetic phases to succeed each other in the same ovotestis, three mutants were studied cytogenetically. Two of the mutants exhibit only the spermatocyte phase and the third shows a greatly reduced and disturbed oogenesis. These three mutations all produce large decreases in ovotestis size and gonocyte number. Each of the three is monofactorial, recessive, autosomal and independent. Homozygous mutant males are also sterile. The gametogenesis phases which could be disturbed by mutation were determined by cytological analysis of the ovotestis of 12 other sterile strains. These phases occur during mitotic divisions of the genital primordium, zygotene chromosome pairing, male meiosis and spermiogenesis, oogenesis induction and oocyte maturation. These steps of gametogenesis need a wild-type genie activity to occur normally. It appears that spermatogenesis and oogenesis are two genetically independent processes, and that oogenesis is rather autonomous and its induction would depend on a hormonal factor.

scholarly journals Sperm Competition in the Absence of Fertilization in Caenorhabditis elegans

Genetics ◽  
1999 ◽  
Vol 152 (1) ◽  
pp. 201-208 ◽  
Author(s):  
Andrew Singson ◽  
Katherine L Hill ◽  
Steven W L’Hernault
Keyword(s):  
Caenorhabditis Elegans ◽  
Sperm Competition ◽  
Sperm Function ◽  
Sperm Precedence ◽  
Wild Type ◽  
Nematode Caenorhabditis Elegans ◽  
C Elegans ◽  
Normal Sperm ◽  
Self Fertilization ◽  
Competition Assays

Abstract Hermaphrodite self-fertilization is the primary mode of reproduction in the nematode Caenorhabditis elegans. However, when a hermaphrodite is crossed with a male, nearly all of the oocytes are fertilized by male-derived sperm. This sperm precedence during reproduction is due to the competitive superiority of male-derived sperm and results in a functional suppression of hermaphrodite self-fertility. In this study, mutant males that inseminate fertilization-defective sperm were used to reveal that sperm competition within a hermaphrodite does not require successful fertilization. However, sperm competition does require normal sperm motility. Additionally, sperm competition is not an absolute process because oocytes not fertilized by male-derived sperm can sometimes be fertilized by hermaphrodite-derived sperm. These results indicate that outcrossed progeny result from a wild-type cross because male-derived sperm are competitively superior and hermaphrodite-derived sperm become unavailable to oocytes. The sperm competition assays described in this study will be useful in further classifying the large number of currently identified mutations that alter sperm function and development in C. elegans.

scholarly journals Genetic, Behavioral and Environmental Determinants of Male Longevity in Caenorhabditis elegans

Genetics ◽  
2000 ◽  
Vol 154 (4) ◽  
pp. 1597-1610 ◽  
Author(s):  
David Gems ◽  
Donald L Riddle
Keyword(s):  
Caenorhabditis Elegans ◽  
Life Span ◽  
Wild Type ◽  
Neuronal Function ◽  
Nematode Caenorhabditis Elegans ◽  
Wild Isolate ◽  
Young Males ◽  
C Elegans ◽  
Single Sex ◽  
Solitary Males

Abstract Males of the nematode Caenorhabditis elegans are shorter lived than hermaphrodites when maintained in single-sex groups. We observed that groups of young males form clumps and that solitary males live longer, indicating that male-male interactions reduce life span. By contrast, grouped or isolated hermaphrodites exhibited the same longevity. In one wild isolate of C. elegans, AB2, there was evidence of copulation between males. Nine uncoordinated (unc) mutations were used to block clumping behavior. These mutations had little effect on hermaphrodite life span in most cases, yet many increased male longevity even beyond that of solitary wild-type males. In one case, the neuronal function mutant unc-64(e246), hermaphrodite life span was also increased by up to 60%. The longevity of unc-4(e120), unc-13(e51), and unc-32(e189) males exceeded that of hermaphrodites by 70–120%. This difference appears to reflect a difference in sex-specific life span potential revealed in the absence of male behavior that is detrimental to survival. The greater longevity of males appears not to be affected by daf-2, but is influenced by daf-16. In the absence of male-male interactions, median (but not maximum) male life span was variable. This variability was reduced when dead bacteria were used as food. Maintenance on dead bacteria extended both male and hermaphrodite longevity.

scholarly journals Isolation, characterization and epistasis of fluoride-resistant mutants of Caenorhabditis elegans.

Genetics ◽  
1994 ◽  
Vol 136 (1) ◽  
pp. 145-154
Author(s):  
I Katsura ◽  
K Kondo ◽  
T Amano ◽  
T Ishihara ◽  
M Kawakami
Keyword(s):  
Caenorhabditis Elegans ◽  
Brood Size ◽  
Normal Growth ◽  
Fluoride Ion ◽  
Wild Type ◽  
Signal Transduction System ◽  
Nematode Caenorhabditis Elegans ◽  
C Elegans ◽  
Class 1 ◽  
Resistant Mutants

Abstract We have isolated 13 fluoride-resistant mutants of the nematode Caenorhabditis elegans. All the mutations are recessive and mapped to five genes. Mutants in three of the genes (class 1 genes: flr-1 X, flr-3 IV, and flr-4 X) are resistant to 400 micrograms/ml NaF. Furthermore, they grow twice as slowly as and have smaller brood size than wild-type worms even in the absence of fluoride ion. In contrast, mutants in the other two genes (class 2 genes: flr-2 V and flr-5 V) are only partially resistant to 400 micrograms/ml NaF, and they have almost normal growth rates and brood sizes in the absence of fluoride ion. Studies on the phenotypes of double mutants showed that class 2 mutations are epistatic to class 1 mutations concerning growth rate and brood size but hypostatic with respect to fluoride resistance. We propose two models that can explain the epistasis. Since fluoride ion depletes calcium ion, inhibits some protein phosphatases and activates trimeric G-proteins, studies on these mutants may lead to discovery of a new signal transduction system that controls the growth of C. elegans.

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 Altered expression of an L1-specific, O-linked cuticle surface glycoprotein in mutants of the nematode Caenorhabditis elegans.

1991 ◽  
Vol 115 (5) ◽  
pp. 1237-1247 ◽  
Author(s):  
R M Hemmer ◽  
S G Donkin ◽  
K J Chin ◽  
D G Grenache ◽  
H Bhatt ◽  
...  
Keyword(s):  
Caenorhabditis Elegans ◽  
Specific Antigen ◽  
Surface Glycoprotein ◽  
Wild Type ◽  
Nematode Caenorhabditis Elegans ◽  
Altered Expression ◽  
C Elegans ◽  
Larval Stages ◽  
Sds Page ◽  
Free Living Nematode

Mouse mAb M38 was used in indirect immunofluorescence experiments to detect a stage-specific antigen on the surface of the first larval stage (L1) of the free-living nematode Caenorhabditis elegans, and to detect alterations in the apparent expression of this antigen in two distinct classes of C. elegans mutants. In previously described srf-2 and srf-3 mutants (Politz S. M., M. T. Philipp, M. Estevez, P.J. O'Brien, and K. J. Chin. 1990. Proc. Natl. Acad. Sci. USA. 87:2901-2905), the antigen is not detected on the surface of any stage. Conversely, in srf-(yj43) and other similar mutants, the antigen is expressed on the surface of the first through the fourth (L4) larval stages. To understand the molecular basis of these alterations, the antigen was characterized in gel immunoblotting experiments. After SDS-PAGE separation and transfer to nitrocellulose, M38 detected a protein antigen in extracts of wild-type L1 populations. The antigen was sensitive to digestion by Pronase and O-glycanase (endo-alpha-N-acetylgalactosaminidase), suggesting that it is an O-linked glycoprotein. This antigen was not detected in corresponding extracts of wild-type L4s or srf-2 or srf-3 L1s, but was detected in extracts of srf-(yj43) L4s. The antigen-defective phenotype of srf-3 was epistatic to the heterochronic mutant phenotype of srf-(yj43) in immunofluorescence tests of the srf-3 srf-(yj43) double mutant, suggesting that srf-(yj43) causes incorrect regulation of a pathway of antigen formation that requires wild-type srf-3 activity.

scholarly journals The PAF1 complex cell-autonomously promotes oogenesis in Caenorhabditis elegans

2021 ◽  
Author(s):  
Yukihiko Kubota ◽  
Natsumi Ota ◽  
Hisashi Takatsuka ◽  
Takuma Unno ◽  
Shuichi Onami ◽  
...  
Keyword(s):  
Caenorhabditis Elegans ◽  
Rna Polymerase Ii ◽  
Oocyte Maturation ◽  
Germ Line ◽  
Biological Processes ◽  
Wild Type ◽  
Expression Of Genes ◽  
A Cell ◽  
Precise Role

The RNA polymerase II-associated factor 1 complex (PAF1C) is a protein complex that consists of LEO1, RTF1, PAF1, CDC73, and CTR9, and has been shown to be involved in Pol II-mediated transcriptional and chromatin regulation. Although it has been shown to regulate a variety of biological processes, the precise role of the PAF1C during germ line development has not been clarified. In this study, we found that reduction in the function of the PAF1C components, LEO-1, RTFO-1, PAFO-1, CDC-73, and CTR-9, in Caenorhabditis elegans affects cell volume expansion of oocytes. Defects in oogenesis were also confirmed using an oocyte maturation marker, OMA-1::GFP. While four to five OMA-1::GFP-positive oocytes were observed in wild-type animals, their numbers were significantly decreased in pafo-1 mutantand leo-1(RNAi), cdc-73(RNAi), and pafo-1(RNAi) animals. Expression of a functional PAFO-1::mCherry transgene in the germline significantly rescued the oogenesis-defective phenotype of the pafo-1 mutants, suggesting that expression of the PAF1C in germ cells is required for oogenesis. Notably, overexpression of OMA-1::GFP partially rescued the oogenesis defect in the pafo-1 mutants. Based on our findings, we propose that the PAF1C promotes oogenesis in a cell-autonomous manner by positively regulating the expression of genes involved in oocyte maturation.

GENETIC STUDIES OF UNUSUAL LOCI THAT AFFECT BODY SHAPE OF THE NEMATODE CAENORHABDITIS ELEGANS AND MAY CODE FOR CUTICLE STRUCTURAL PROTEINS

Genetics ◽  
1986 ◽  
Vol 113 (3) ◽  
pp. 621-639
Author(s):  
Meredith Kusch ◽  
R S Edgar
Keyword(s):  
Caenorhabditis Elegans ◽  
Body Shape ◽  
Structural Proteins ◽  
Null Alleles ◽  
Wild Type ◽  
Nematode Caenorhabditis Elegans ◽  
Genetic Studies ◽  
Wild Type Phenotype ◽  
Mutant Phenotypes ◽  
Collagen Genes

ABSTRACT In Caenorhabditis elegans, four loci (sqt-1, sqt-2, sqt-3 and rol-8) in which mutations affect body shape and cuticle morphology have unusual genetic properties. (1) Mutant alleles of sqt-1 can interact to produce animals with a variety of mutant phenotypes: left roller, right roller, dumpy and long. At least three mutant phenotypes are specified by mutations in the sqt-3 locus. (2) Most alleles at these loci are either dominant or cryptic dominant (i.e., are dominant only in certain genetic backgrounds). (3) Most alleles of these loci exhibit codominance. (4) Two putative null alleles of the sqt-1 locus produce a wild-type phenotype. (5) Many alleles of these genes demonstrate unusual intergenic interactions that are not the result of simple epistasis: animals doubly heterozygous for mutations at two loci often display unexpected and unpredictable phenotypes. We suggest that these genetic properties might be expected of genes, such as the collagen genes, the products of which interact to form the animal's cuticle, and which are member genes of a gene family.

MUTATIONS WITH DOMINANT EFFECTS ON THE BEHAVIOR AND MORPHOLOGY OF THE NEMATODE CAENORHABDITIS ELEGANS

Genetics ◽  
1986 ◽  
Vol 113 (4) ◽  
pp. 821-852
Author(s):  
Eun-Chung Park ◽  
H Robert Horvitz
Keyword(s):  
Caenorhabditis Elegans ◽  
Random Sample ◽  
Gene Function ◽  
The Novel ◽  
Wild Type ◽  
Nematode Caenorhabditis Elegans ◽  
Type Function ◽  
C Elegans ◽  
Wild Type Phenotype ◽  
Gene Functions

ABSTRACT We have analyzed 31 mutations that have dominant effects on the behavior or morphology of the nematode Caenorhabditis elegans. These mutations appear to define 15 genes. We have studied ten of these genes in some detail and have been led to two notable conclusions. First, loss of gene function for four of these ten genes results in a wild-type phenotype; if these genes represent a random sample from the genome, then we would estimate that null mutations in about half of the genes in C. elegans would result in a nonmutant phenotype. Second, the dominant effects of mutations in nine of these ten genes are caused by novel gene functions, and in all nine cases the novel function is antagonized by the wild-type function.

scholarly journals Dephosphorylation of Cell Cycle–regulated Proteins Correlates with Anoxia-induced Suspended Animation in Caenorhabditis elegans

2002 ◽  
Vol 13 (5) ◽  
pp. 1473-1483 ◽  
Author(s):  
Pamela A. Padilla ◽  
Todd G. Nystul ◽  
Richard A. Zager ◽  
Ali C.M. Johnson ◽  
Mark B. Roth
Keyword(s):  
Cell Cycle ◽  
Caenorhabditis Elegans ◽  
Wild Type ◽  
Suspended Animation ◽  
Nematode Caenorhabditis Elegans ◽  
Phosphorylation State ◽  
Cellular Processes ◽  
Developmental Progression ◽  
Energetic State ◽  
Specific Proteins

Some metazoans have evolved the capacity to survive severe oxygen deprivation. The nematode, Caenorhabditis elegans, exposed to anoxia (0 kPa, 0% O2) enters into a recoverable state of suspended animation during all stages of the life cycle. That is, all microscopically observable movement ceases including cell division, developmental progression, feeding, and motility. To understand suspended animation, we compared oxygen-deprived embryos to nontreated embryos in both wild-type and hif-1 mutants. We found that hif-1 mutants survive anoxia, suggesting that the mechanisms for anoxia survival are different from those required for hypoxia. Examination of wild-type embryos exposed to anoxia show that blastomeres arrest in interphase, prophase, metaphase, and telophase but not anaphase. Analysis of the energetic state of anoxic embryos indicated a reversible depression in the ATP to ADP ratio. Given that a decrease in ATP concentrations likely affects a variety of cellular processes, including signal transduction, we compared the phosphorylation state of several proteins in anoxic embryos and normoxic embryos. We found that the phosphorylation state of histone H3 and cell cycle–regulated proteins recognized by the MPM-2 antibody were not detectable in anoxic embryos. Thus, dephosphorylation of specific proteins correlate with the establishment and/or maintenance of a state of anoxia-induced suspended animation.

Comparative analysis of female and male meiosis in three meiotic mutants of tomato

Genome ◽  
1997 ◽  
Vol 40 (6) ◽  
pp. 879-886 ◽  
Author(s):  
Francis W. J. Havekes ◽  
J. Hans de Jong ◽  
Christa Heyting
Keyword(s):  
Comparative Analysis ◽  
Chromosome Pairing ◽  
Meiotic Prophase ◽  
Chiasma Frequency ◽  
Chiasma Formation ◽  
Male Meiosis ◽  
Wild Type ◽  
Female Meiosis ◽  
Similar Reduction ◽  
Meiotic Mutants

Female meiosis was analysed in squash preparations of ovules from three meiotic mutants and wild-type plants of tomato. In the completely asynaptic mutant as6, chromosome pairing and chiasma formation were virtually absent in both sexes. In the partially asynaptic mutant asb, with intermediate levels of chromosome pairing at pachytene, there were a higher number of chiasmate chromosome arms in female meiosis than in male meiosis, whereas in the desynaptic mutant as5 there were normal levels of chromosome pairing at pachytene and a similar reduction in chiasma frequency in the two sexes. In wild-type tomato, we found slightly higher numbers of chiasmate chromosome arms in female meiosis than in male meiosis. We propose that the higher female chiasma frequencies in mutant asb and wild-type tomato result from a longer duration of female meiotic prophase. This would allow chromosomes more time to pair and recombine. It is possible that a longer duration of prophase I does not affect mutants as5 and as6, either because the meiotic defect acts before the pairing process begins (in as6) or because it acts at a later stage and involves chiasma maintenance (in as5).Key words: female meiosis, tomato, chiasma, mutant.

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