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[
Commun Integr Biol,
2010]
Wolbachia pipientis is known to infect only arthropods and nematodes (mainly filarial worms). A unique feature shared by the two Phyla is the ability to replace the exoskeleton, a process known as ecdysis. This shared characteristic is thought to reflect a common ancestry. Arthropod moulting is induced by the steroid hormone 20-hydroxyecdysone (20E) and a role for ecdysteroids in nematode ecdysis has also been suggested. Removing Wolbachia from filarial worms impairs the host's development. From analyses of the genome of Wolbachia harbored by the filarial nematode Brugia malayi and that of its host, the bacterium may provide a source of heme, an essential component of cytochrome P450's that are necessary for steroid hormone biosynthetic pathways.In arthropods, Wolbachia is a reproductive manipulator, inducing various phenotypic effects that may be due to differences in host physiology, in particular, endocrine-related processes governing development and reproduction. Insect steroids have well-defined roles in the coordination of multiple developmental processes, and in adults they control important aspects of reproduction, including ovarian development, oogenesis, sexual behavior, and in some taxa vitellogenin biosynthesis.According to some authors ecdysteroids may also act as sex hormones. In insects sex differentiation is generally thought to be a strictly genetic process, in which each cell decides its own sexual fate based on its sex chromosome constitution, but, surprisingly, recent data demonstrate that in Drosophila sex determination is not cell-autonomous, as it happens in mammals. Thus the presence of signals coordinating the development of a gender-specific phenotype cannot be excluded.This could explain why Wolbachia interferes with insect reproduction; and also could explain why Wolbachia interferes with insect development.Thus, is "sex (=reproduction) and stripping (=ecdysis)" the key to the intimate relationship between Wolbachia and its host?
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[
Int J Parasitol,
2004]
Wolbachia pipientis is a bacterial endosymbiont associated with arthropods and filarial nematodes. In filarial nematodes, W. pipientis has been shown to play an important role in the biology of the host and in the immuno-pathology of filariasis. Several species of filariae, including the most important parasites of humans and animals (e.g. Onchocerca volvulus, Wuchereria bancrofti and Dirofilaria immitis) have been shown to harbour these bacteria. Other filarial species, including an important rodent species (Acanthocheilonema viteae), which has been used as a model for the study of filariasis, do not appear to harbour these symbionts. There are still several open questions about the distribution of W. pipientis in filarial nematodes. Firstly the number of species examined is still limited. Secondly, it is not clear whether the absence of W. pipientis in negative species could represent an ancestral characteristic or the result of a secondary loss. Thirdly, several aspects of the phylogeny of filarial nematodes are still unclear and it is thus difficult to overlay the presence/absence of W. pipientis on a tree representing filarial evolution. Here we present the results of a PCR screening for W. pipientis in 16 species of filariae and related nematodes, representing different families/subfamilies. Evidence for the presence of W. pipientis is reported for five species examined for the first time (representing the genera Litomosoides, Litomosa and Dipetalonema); original results on the absence of this bacterium are reported for nine species; for the remaining two species, we have confirmed the absence of W. pipientis recently reported by other authors. In the positive species, the infecting W. pipientis bacteria have been identified through 16S rDNA gene sequence analysis. In addition to the screening for W. pipientis in 16 species, we have generated phylogenetic reconstructions based on mitochondrial gene sequences (12S rDNA; COI), including a total of 28 filarial species and related spirurid nematodes. The mapping of the presence/absence of W. pipientis on the trees generated indicates that these bacteria have possibly been lost during evolution along some lineages of filarial nematodes.
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[
Parasitology,
2010]
Up to 5% of untreated female Onchocerca volvulus filariae develop potentially fatal pleomorphic neoplasms, whose incidence is increased following ivermectin treatment. We studied the occurrence of 8 filarial proteins and of Wolbachia endobacteria in the tumor cells. Onchocercomas from patients, untreated and treated with antibiotics and anthelminthics, were examined by immunohistology. Neoplasms were diagnosed in 112 of 3587 female and in 2 of 1570 male O. volvulus. The following proteins and other compounds of O. volvulus were expressed in the cells of the neoplasms: glutathione S-transferase 1, lysosomal aspartic protease, cAMP-dependent protein kinase, alpha-enolase, aspartate aminotransferase, ankyrin E1, tropomyosin, heat shock protein 60, transforming growth factor-beta, and prostaglandin E(2). These findings prove the filarial origin of the neoplasms and confirm the pleomorphism of the tumor cells. Signs indicating malignancy of the neoplasms are described. Wolbachia were observed in the hypodermis, oocytes, and embryos of tumor-harbouring filariae using antibodies against Wolbachia surface protein, Wolbachia HtrA-type serine protease, and Wolbachia aspartate aminotransferase. In contrast, Wolbachia were not found in the cells of the neoplasms. Further, neoplasm-containing worms were not observed after more than 10 months after the start of sufficient treatment with doxycycline or doxycycline plus ivermectin.
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[
BMC Genomics,
2007]
ABSTRACT: BACKGROUND: In the genome of Caenorhabditis elegans, homopolymeric poly-G/poly-C tracts (G/C tracts) exist at high frequency and are maintained by the activity of the DOG-1 protein. The frequency and distribution of G/C tracts in the genomes of C. elegans and the related nematode, C. briggsae were analyzed to investigate possible biological roles for G/C tracts. RESULTS: In C. elegans, G/C tracts are distributed along every chromosome in a non-random pattern. Most G/C tracts are within introns or are close to genes. Analysis of SAGE data showed that G/C tracts correlate with the levels of regional gene expression in C. elegans. G/C tracts are over-represented and dispersed across all chromosomes in another Caenorhabditis species, C. briggase. However, the positions and distribution of G/C tracts in C. briggsae differ from those in C. elegans. Furthermore, the C. briggsae
dog-1 ortholog CBG19723 can rescue the mutator phenotype of C. elegans
dog-1 mutants. CONCLUSIONS: The abundance and genomic distribution of G/C tracts in C. elegans, the effect of G/C tracts on regional transcription levels, and the lack of positional conservation of G/C tracts in C. briggsae suggest a role for G/C tracts in chromatin structure but not in the transcriptional regulation of specific genes.
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Horng JC, Hsu HL, Nazilah KR, Wang CC, Wang TL, Wang SC, Antika TR, Chuang TH, Chrestella DJ, Wang SW, Tseng YK, Pan HC
[
J Biol Chem,
2023]
Alanyl-tRNA synthetase (AlaRS) retains a conserved prototype structure throughout its biology. Nevertheless, its C-terminal domain (C-Ala) is highly diverged and has been shown to play a role in either tRNA or DNA binding. Interestingly, we discovered that Caenorhabditis elegans cytoplasmic C-Ala (Ce-C-Ala<sub>c</sub>) robustly binds both ligands. How Ce-C-Ala<sub>c</sub> targets its cognate tRNA and whether a similar feature is conserved in its mitochondrial counterpart remain elusive. We show that the N- and C-terminal subdomains of Ce-C-Ala<sub>c</sub> are responsible for DNA and tRNA binding, respectively. Ce-C-Ala<sub>c</sub> specifically recognized the conserved invariant base G<sup>18</sup> in the D-loop of tRNA<sup>Ala</sup> through a highly conserved lysine residue, K934. Despite bearing little resemblance to other C-Ala domains, C. elegans mitochondrial C-Ala (Ce-C-Ala<sub>m</sub>) robustly bound both tRNA<sup>Ala</sup> and DNA and maintained targeting specificity for the D-loop of its cognate tRNA. This study uncovers the underlying mechanism of how C. elegans C-Ala specifically targets the D-loop of tRNA<sup>Ala</sup>.
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[
Journal of Thermal Biology,
1995]
1. The patterns of HSP70 expression induced in Caenorhabditis elegans by mild (31 degrees C) or severe (34 degrees C) heat shock, and by cadmium ions at 31 degrees C, have been compared with those expressed constitutively ill 20 degrees C controls by 1- and a-dimensional immunoblotting. 2. The 2D spot patterns become more complex with increasing severity of stress (34 degrees C > 31 degrees C + Cd > 31 degrees C > 20 degrees C). 3. A stress-inducible transgene construct is minimally active at 31 degrees C, but is abundantly expressed in the presence of cadmium or at 34 degrees C. 4. Differing degrees or types of stress may differentially induce available
hsp70 -
[
J Nanosci Nanotechnol,
2018]
Uniform and hydrophilic carbon quantum dots (C-QDs) were synthesized by calcination and NaOH treatment from an organo-templated zeolite precursor. The color of luminescence was determined by the concentration of C-QDs. These variable-color C-QDs were applied for the first time in the imaging of Caenorhabditis elegans (C. elegans) as a model organism. The effects of C-QDs and possible behavioral changes in C. elegans were evaluated under treatment conditions. We could clearly observe distribution of C-QDs in C. elegans from the fluorescence images. Furthermore, we observed significant and detectable fluorescence quenching of the C-QDs by free radicals in C. elegans. Our work affirms that C-QDs can be developed as imaging probes and as potential fluorescent quantitative probes for detecting free radicals.
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[
Mol Immunol,
2021]
Candida albicans is an opportunistic fungal human pathogen that has been causing an increasing number of deaths each year. Due to the widespread use of broad-spectrum antibiotics and immunosuppressants, C. albicans resistance to these therapies has increased. Thus, natural plant inhibitors are being investigated for treating C. albicans infections. Schinifoline is a 4-quinolinone alkaloid with antibacterial, insecticidal, antitumor, and other biological activities. Here, we explored the effects of schinifoline on C. albicans in C. elegans and extracted RNA from uninfected C. elegans, C. elegans infected with C. albicans, and C. elegans infected with C. albicans and treated with 100 mg/l schinifoline. Our results showed that there were significant differences among the three groups. The GO and KEGG pathway analysis suggested that the pathogenicity of C. albicans to C. elegans was caused by abnormal protein function. Schinifoline regulates lysosomal pathway related genes that accelerate the metabolism and degradation of abnormal proteins, thereby inhibiting the negative effects of C. albicans in vivo. These findings advance our understanding of the molecular mechanisms underlying schinifoline inhibition of C. albicans.
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[
Cell,
1993]
In insects and vertebrates, clusters of Antennapedia class homeobox (HOM-C) genes specify anteroposterior body pattern. The nematode C. elegans also contains a small cluster of HOM-C genes, one of which has been shown to specify positional identity. Here we show that two additional C. elegans HOM-C genes also specify positional identity and that together these three HOM-C genes function along the anteroposterior axis in the same order as their homologs in other organisms. Thus, HOM-C-based pattern formation has been conserved in nematodes despite the many differences in morphology and embryology that distinguish them from other phyla. Each C. elegans HOM-C gene is responsible for a distinct body region; however, where their domains overlap, two HOM-C genes can act together to specify the fates of individual cells.
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[
New Microbiol,
2022]
Candida albicans can cause infections ranging from superficial skin infections to life-threateningsystemic infections in immunocompromised hosts. Although several C. albicans virulence factorsare widely discussed in great detail, intrinsic host determinants that are critical for C. albicanspathogenesis remain less interested and poorly understood. In view of this, a model of Caenorhabditiselegans was used to study host longevity and immunity in response to C. albicans pathogenesis.The influence of C. albicans in pathological and survival aspects was evaluated using C. elegans.C. albicans hyphal formation in different C. elegans genetic backgrounds was evaluated. Moreover,several C. elegans fluorescent proteins as gene expression markers upon C. albicans infectionswere evaluated. C. albicans is pathogenic to C. elegans and reduces the lifespan of C. elegans inassociation with repression of the insulin/IGF-1-like signaling (IIS) pathway. Moreover, repressionof DAF-16/forkhead transcription factor increases aggressiveness of C. albicans by enhancing hyphalformation. In addition, infection of C. albicans increases lipofuscin accumulation, promotes DAF-16nuclear translocation, increases superoxide dismutase (SOD-3) expression, which coordinately linksbetween aging and innate immunity. Thus, we demonstrate here the strategy to utilize C. elegans asa model host to elucidate host genetic determinants that provide insights into the pathogenesis ofC. albicans infections.