Habacher C et al. (2016) Dev Cell "Ribonuclease-Mediated Control of Body Fat."

Harvald EB, Gaidatzis D, Neagu A, Habacher C, Venz R, Ciosk R, Kumari P, Gut H, Faergeman NJ, Guo Y

[Dev Cell, 2016]

Obesity is a global health issue, arousing interest in molecular mechanisms controlling fat. Transcriptional regulation of fat has received much attention, and key transcription factors involved in lipid metabolism, such as SBP-1/SREBP, LPD-2/C/EBP, and MDT-15, are conserved from nematodes to mammals. However, there is a growing awareness that lipid metabolism can also be controlled by post-transcriptional mechanisms. Here, we show that the Caenorhabditis elegans RNase, REGE-1, related to MCPIP1/Zc3h12a/Regnase-1, a key regulator of mammalian innate immunity, promotes accumulation of body fat. Using exon-intron split analysis, we find that REGE-1 promotes fat by degrading the mRNA encoding ETS-4, a fat-loss-promoting transcription factor. Because ETS-4, in turn, induces rege-1 transcription, REGE-1 and ETS-4 appear to form an auto-regulatory module. We propose that this type of fat regulation may be of key importance when, if faced with an environmental change, an animal must rapidly but precisely remodel its metabolism.

Woglar A et al. (2013) PLoS Genet "Matefin/SUN-1 phosphorylation is part of a surveillance mechanism to coordinate chromosome synapsis and recombination with meiotic progression and chromosome movement."

Habacher C, La Volpe A, Daryabeigi A, Jantsch V, Adamo A, Machacek T, Woglar A

[PLoS Genet, 2013]

Faithful chromosome segregation during meiosis I depends on the establishment of a crossover between homologous chromosomes. This requires induction of DNA double-strand breaks (DSBs), alignment of homologs, homolog association by synapsis, and repair of DSBs via homologous recombination. The success of these events requires coordination between chromosomal events and meiotic progression. The conserved SUN/KASH nuclear envelope bridge establishes transient linkages between chromosome ends and cytoskeletal forces during meiosis. In Caenorhabditis elegans, this bridge is essential for bringing homologs together and preventing nonhomologous synapsis. Chromosome movement takes place during synapsis and recombination. Concomitant with the onset of chromosome movement, SUN-1 clusters at chromosome ends associated with the nuclear envelope, and it is phosphorylated in a chk-2- and plk-2-dependent manner. Identification of all SUN-1 phosphomodifications at its nuclear N terminus allowed us to address their role in prophase I. Failures in recombination and synapsis led to persistent phosphorylations, which are required to elicit a delay in progression. Unfinished meiotic tasks elicited sustained recruitment of PLK-2 to chromosome ends in a SUN-1 phosphorylation-dependent manner that is required for continued chromosome movement and characteristic of a zygotene arrest. Furthermore, SUN-1 phosphorylation supported efficient synapsis. We propose that signals emanating from a failure to successfully finish meiotic tasks are integrated at the nuclear periphery to regulate chromosome end-led movement and meiotic progression. The single unsynapsed X chromosome in male meiosis is precluded from inducing a progression delay, and we found it was devoid of a population of phosphorylated SUN-1. This suggests that SUN-1 phosphorylation is critical to delaying meiosis in response to perturbed synapsis. SUN-1 may be an integral part of a checkpoint system to monitor establishment of the obligate crossover, inducible only in leptotene/zygotene. Unrepaired DSBs and unsynapsed chromosomes maintain this checkpoint, but a crossover intermediate is necessary to shut it down.

Zhao Y et al. (2007) BMC Genomics "Poly-G/poly-C tracts in the genomes of Caenorhabditis."

Zhao Y, O'Neil NJ, Rose AM

[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.

Antika TR et al. (2023) J Biol Chem "Sequence-specific targeting of C. elegans C-Ala to the D-loop of tRNAAla."

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_c) robustly binds both ligands. How Ce-C-Ala_c 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_c are responsible for DNA and tRNA binding, respectively. Ce-C-Ala_c specifically recognized the conserved invariant base G¹⁸ in the D-loop of tRNA^Ala through a highly conserved lysine residue, K934. Despite bearing little resemblance to other C-Ala domains, C. elegans mitochondrial C-Ala (Ce-C-Ala_m) robustly bound both tRNA^Ala 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^Ala.

Guven K (1995) Journal of Thermal Biology "Differential expression of hsp70 proteins in response to heat and cadmium in Caenorhabditis elegans."

Guven K

[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

Xu J et al. (2018) J Nanosci Nanotechnol "Carbon Quantum Dots as Fluorescent Probes for Imaging and Detecting Free Radicals in C. elegans."

Wang Q, Guan S, Wang L, Wang M, Zhang Y, Mu Y, Xu J, Wang K, Li J

[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.

Lu L et al. (2021) Mol Immunol "Whole transcriptome analysis of schinifoline treatment in Caenorhabditis elegans infected with Candida albicans."

Shu C, Ma S, Li S, Li Z, Shan C, Chen G, Lu L, Nie W, Wang H

[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.

Wang BB et al. (1993) Cell "A homeotic gene cluster patterns the anteroposterior body axis of C. elegans."

Wang BB, Kenyon CJ, Robinson NT, Chisholm AD, Austin JA, Mueller-Immergluck MM

[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.

Kitisin T et al. (2022) New Microbiol "Regulation of DAF-16-mediated longevity and immune response to Candida albicans infection in Caenorhabditis elegans."

Kitisin T, Sukphopetch P, Muangkaew W

[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.

Li R et al. (2015) Mitochondrial DNA "Mitochondrial genome of Caenorhabditis nigoni (Rhabditida: Rhabditidae)."

Bi Y, Zhao Z, Ren X, Li R

[Mitochondrial DNA, 2015]

Abstract To facilitate comparative genomic study in the Caenorhabditis species, the mitochondrial genome (mitogenome) of a nematode species Caenorhabditis nigoni (previous name: Caenorhabditis sp. 9) was generated using next-generation sequencing. The mitogenome length is 13,413bp, containing 12 protein-coding genes (PCGs), 2 ribosomal RNA genes (rRNAs), 22 transfer RNA genes (tRNAs) and 2 non-coding regions (NCR). The genome organization and nucleotide composition is very similar to that of the mitogenome of C. elegans and C. briggsae. Mitogenome of C. nigoni shows higher sequence similarity to C. briggsae than to C. elegans, which is consistent with the fact that C. nigoni is a sister species of C. briggsae. However, as in C. elegans, two NCRs present in the mitogenome of C. briggsae are missing in C. nigoni. The mitogenome sequence of C. nigoni plays an important role in further studies of phylogenetics, population genetics and evolutionary genetics in nematode species.