The synaptonemal complexes of Caenorhabditis elegans: pachytene karyotype analysis of male and hermaphrodite wild-type and him mutants

Chromosoma ◽  
1982 ◽  
Vol 86 (4) ◽  
pp. 577-593 ◽  
Author(s):  
Paul Goldstein
Keyword(s):  
Caenorhabditis Elegans ◽  
Karyotype Analysis ◽  
Wild Type ◽  
Synaptonemal Complexes ◽  
Pachytene Karyotype

Triplo-X hermaphrodite of Caenorhabditis elegans: pachytene karyotype analysis, synaptonemal complexes, and pairing mechanisms

1984 ◽  
Vol 26 (1) ◽  
pp. 13-17 ◽  
Author(s):  
Paul Goldstein
Keyword(s):  
Caenorhabditis Elegans ◽  
Karyotype Analysis ◽  
Real Difference ◽  
X Chromosomes ◽  
Synaptonemal Complexes ◽  
Chromosomal Complement ◽  
Male Line ◽  
Pachytene Karyotype

Pairing of the three X chromosomes in the triplo-X strain of Caenorhabditis elegans occurs at pachytene in a two-by-two fashion such that one bivalent and one univalent are formed. The XX bivalent pairs synchronously with the autosomes and the univalent X remains in a similar chromatic state as the rest of the chromosomal complement. Normal tripartite synaptonemal complexes (SC) are formed between all bivalents. The univalent X lacks a SC and an axial core is not observed. The condensation of the univalent X in the triplo-X is different than in the male where the univalent X is heterochromatic. This real difference in condensation states of the chromatin may explain the fact that the univalent X is maintained in the male line yet it is easily lost in the triplo-X strain.

The synaptonemal complexes of Caenorhabditis elegans: pachytene karyotype analysis of hermaphrodites from the recessive him-5 and him-7 mutants

1986 ◽  
Vol 82 (1) ◽  
pp. 119-127
Author(s):  
P. Goldstein
Keyword(s):  
Caenorhabditis Elegans ◽  
X Chromosome ◽  
High Frequency ◽  
Karyotype Analysis ◽  
Nuclear Morphology ◽  
Group V ◽  
Haploid Chromosome Number ◽  
High Incidence ◽  
Physical Position ◽  
Pachytene Karyotype

The him-5 and him-7 mutants (high incidence of males) of Caenorhabditis elegans both showed increased rates of X chromosome non-disjunction (16% and 3%, respectively) but him-7 also had a high frequency of autosomal non-disjunction (34%). Synaptonemal complex (SC) karyotype analysis revealed a haploid chromosome number of six in each strain. Alterations in him-7 nuclear morphology were observed but there were no aberrations in SC structure that could account for the increased frequency of autosomal non-disjunction. However, the frequency of X-chromosome non-disjunction occurred at predicted rates on the basis of the number of disjunction regulator regions (DRRs) present on the SCs. The observation that the levels of X-chromosome non-disjunction were not influenced by the increase in the frequency of autosomal non-disjunction supports the notion that the X chromosome is subject to separate controls during meiosis. The him-7 mutant is nested within the rad-4 map region on linkage group V, however, SC analysis did not reveal the physical position on the chromosome because of synaptic adjustment.

The synaptonemal complexes of Caenorhabditis elegans: duplication mutants sDp1 and mnDp1, disjunction regulator regions and aneuploidy

Nematology ◽  
2010 ◽  
Vol 12 (5) ◽  
pp. 759-766
Author(s):  
Paul Goldstein
Keyword(s):  
Caenorhabditis Elegans ◽  
Linkage Group ◽  
X Chromosome ◽  
Initiation Site ◽  
Genetic Maps ◽  
Wild Type ◽  
Pachytene Nucleus ◽  
Synaptonemal Complexes ◽  
Recombination Nodules ◽  
Group I

AbstractThe duplication mutants sDp1 and mnDp1 in Caenorhabditis elegans differ in their size and recombination/pairing strategies within the pachytene nucleus. mnDp1 is a duplication of approximately 18% of the X chromosome with the duplicated segment transposed and inserted into linkage group V. sDp1 is a free duplication which covers 30 map units of linkage group I and crossing-over has been determined genetically with its homologue. Analysis of the synaptonemal complexes (SC) and pachytene karyotypes of both duplication mutants reveal that there is an extension of one of the SCs in mnDp1 while the sDp1 free duplication partially pairs with its homologue along a small portion of its length. The remaining region exists as a univalent in the pachytene nucleus. This indicates that there is at least one SC initiation site on the sDp1 free duplication. Only bivalent pairing is permitted and there are no trivalents. To some extent, the autosomes preferentially pair at the exclusion of the sDp1 duplication. Switching of pairing partners was evident between the duplication and the homologue, probably because of the size of the duplication. Thus, the mechanism of chromosome segregation in the two duplications is different. The number of Disjunction Regulator Regions, which are associated with X-chromosome nondisjunction, was three in both mutants compared to six in wild-type. The number of males produced in mnDp1 was 1.0%, in sDp1 it was 2.0%, while in wild-type it is 0.3%. Recombination nodules were not observed in any nuclei. The ultimate goal of these studies is to correlate the physical and genetic maps and in this study linkage group I has been identified in the pachytene nucleus.

The Effect of Mianserin on Lifespan of Caenorhabditis elegans is Abolished by Glucose

2021 ◽  
Vol 13 ◽  
Author(s):  
Abdullah Almotayri ◽  
Jency Thomas ◽  
Mihiri Munasinghe ◽  
Markandeya Jois
Keyword(s):  
Caenorhabditis Elegans ◽  
Scaffolding Protein ◽  
Lifespan Extension ◽  
Wild Type ◽  
E Coli ◽  
C Elegans ◽  
Risk Of Death ◽  
Increased Risk ◽  
Antidepressant Use ◽  
Extension Effect

Background: The antidepressant mianserin has been shown to extend the lifespan of Caenorhabditis elegans (C. elegans), a well-established model organism used in aging research. The extension of lifespan in C. elegans was shown to be dependent on increased expression of the scaffolding protein (ANK3/unc-44). In contrast, antidepressant use in humans is associated with an increased risk of death. The C. elegans in the laboratory are fed Escherichia coli (E. coli), a diet high in protein and low in carbohydrate, whereas a typical human diet is high in carbohydrates. We hypothesized that dietary carbohydrates might mitigate the lifespan-extension effect of mianserin. Objective: To investigate the effect of glucose added to the diet of C. elegans on the lifespan-extension effect of mianserin. Methods: Wild-type Bristol N2 and ANK3/unc-44 inactivating mutants were cultured on agar plates containing nematode growth medium and fed E. coli. Treatment groups included (C) control, (M50) 50 μM mianserin, (G) 73 mM glucose, and (M50G) 50 μM mianserin and 73 mM glucose. Lifespan was determined by monitoring the worms until they died. Statistical analysis was performed using the Kaplan-Meier version of the log-rank test. Results: Mianserin treatment resulted in a 12% increase in lifespan (P<0.05) of wild-type Bristol N2 worms but reduced lifespan by 6% in ANK3/unc-44 mutants, consistent with previous research. The addition of glucose to the diet reduced the lifespan of both strains of worms and abolished the lifespan-extension by mianserin. Conclusion: The addition of glucose to the diet of C. elegans abolishes the lifespan-extension effects of mianserin.

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.

Streblus asper Lour. exerts MAPK and SKN-1 mediated anti-aging, anti-photoaging activities and imparts neuroprotection by ameliorating Aβ in Caenorhabditis elegans

2021 ◽  
pp. 1-17
Author(s):  
Mani Iyer Prasanth ◽  
James Michael Brimson ◽  
Dicson Sheeja Malar ◽  
Anchalee Prasansuklab ◽  
Tewin Tencomnao
Keyword(s):  
Oxidative Stress ◽  
Caenorhabditis Elegans ◽  
Stress Resistance ◽  
Vital Role ◽  
Transgenic Strain ◽  
Wild Type ◽  
Neuroprotective Effects ◽  
C Elegans ◽  
Streblus Asper

BACKGROUND: Streblus asper Lour., has been reported to have anti-aging and neuroprotective efficacies in vitro. OBJECTIVE: To analyze the anti-aging, anti-photoaging and neuroprotective efficacies of S. asper in Caenorhabditis elegans. METHODS: C. elegans (wild type and gene specific mutants) were treated with S. asper extract and analyzed for lifespan and other health benefits through physiological assays, fluorescence microscopy, qPCR and Western blot. RESULTS: The plant extract was found to increase the lifespan, reduce the accumulation of lipofuscin and modulate the expression of candidate genes. It could extend the lifespan of both daf-16 and daf-2 mutants whereas the pmk-1 mutant showed no effect. The activation of skn-1 was observed in skn-1::GFP transgenic strain and in qPCR expression. Further, the extract can extend the lifespan of UV-A exposed nematodes along with reducing ROS levels. Additionally, the extract also extends lifespan and reduces paralysis in Aβ transgenic strain, apart from reducing Aβ expression. CONCLUSIONS: S. asper was able to extend the lifespan and healthspan of C. elegans which was independent of DAF-16 pathway but dependent on SKN-1 and MAPK which could play a vital role in eliciting the anti-aging, anti-photoaging and neuroprotective effects, as the extract could impart oxidative stress resistance and neuroprotection.

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.

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