Dlakic M (2002) Curr Biol "A new family of putative insulin receptor-like proteins in C. elegans."

Dlakic M

[Curr Biol, 2002]

Delayed senescence in C. elegans is controlled by an insulin receptor-like gene which regulates both reproductive development and metabolism in a manner similar to the corresponding mammalian pathway. However, despite the large number of insulin-like ligands in C. elegans, only one protein has been identified.

Rajaram S et al. (2000) Genesis "The sequence and associated null phenotype of a C. elegans neurocalcin-like gene."

Sedensky MM, Rajaram S, Morgan PG

[Genesis, 2000]

The neuronal calcium sensor (NCS) proteins belong to a subfamily of the EF-hand calcium binding proteins. These proteins are primarily expressed in the nervous system and currently include more than 20 members across species [Nakayama et al., J Mol Evol 34:416-448, 1992]. Two homologues of the ncs genes, Ce-ncs-1 and Ce-ncs-2, have recently been identified in the nematode C. elegans. Here we report the cDNA sequence of a third C. elegans ncs homologue, Ce-ncs-3. We demonstrate that a null mutation in this gene caused by a large deletion in the locus does not confer a visible phenotype in C. elegans. This, in addition to the strong homology between Ce-NCS-3 and the other C. elegans NCS proteins, may indicate functional redundancy between the three genes.

Murphey AC et al. (2018) FEBS Lett "The heme auxotroph Caenorhabditis elegans can cleave the thioether bonds of c-type cytochromes."

Mavridou DAI, Ferguson SJ, Murphey AC, Hodgkin J

[FEBS Lett, 2018]

Heme is essential and synthesised via highly-regulated processes. For this reason, most organisms strive to recycle it or acquire it from their environment. When heme is bound to proteins non-covalently, degradation of the polypeptide is sufficient to release it. However, in some hemoproteins, such as c-type cytochromes, heme is covalently bound to the protein backbone. We use the heme auxotroph Caenorhabditis elegans to investigate if cytochromes c can be a heme source, and we show that this organism must encode a novel system, which specifically cleaves the thioether bonds of c-type cytochromes. We also find that at limiting heme concentrations, while somatic tissues develop normally the germline fails to proliferate, suggesting the presence of a heme-sensing checkpoint in C. elegans. This article is protected by copyright. All rights reserved.

Voell MR et al. (2010) BMC Genomics "A response to Rome: lessons from pre- and post-publication data-sharing in the C. elegans research community."

Farris L, Voell MR, Levy E, Marden E

[BMC Genomics, 2010]

BACKGROUND: In recent years numerous studies have undertaken to measure the impact of patents, material transfer agreements, data-withholding and commercialization pressures on biomedical researchers. Of particular concern is the theory that such pressures may have negative effects on academic and other upstream researchers. In response to these concerns, commentators in some research communities have called for an increased level of access to, and sharing of, data and research materials. We have been studying how data and materials are shared in the community of researchers who use the nematode Caenorhabditis elegans (C. elegans) as a model organism for biological research. Specifically, we conducted a textual analysis of academic articles referencing C. elegans, reviewed C. elegans repository request lists, scanned patents that reference C. elegans and conducted a broad survey of C. elegans researchers. Of particular importance in our research was the role of the C. elegans Gene Knockout Consortium in the facilitation of sharing in this community. RESULTS: Our research suggests that a culture of sharing exists within the C. elegans research community. Furthermore, our research provides insight into how this sharing operates and the role of the culture that underpins it. CONCLUSIONS: The greater scientific community is likely to benefit from understanding the factors that motivate C. elegans researchers to share. In this sense, our research is a 'response' to calls for a greater amount of sharing in other research communities, such as the mouse community, specifically, the call for increased investment and support of centralized resource sharing infrastructure, grant-based funding of data-sharing, clarity of third party recommendations regarding sharing, third party insistence of post-publication data sharing, a decrease in patenting and restrictive material transfer agreements, and increased attribution and reward.

Ausubel FM et al. (2004) Science "Bacterial resistance of daf-2 mutants - response."

Sifri CD, Kim DH, Moy T, Begun J, Calderwood SB, Garsin DA, Ruvkun G, Ausubel FM

[Science, 2004]

Bolm et al. raise an important issue that we have considered as well. Because many streptococcal species are able to quickly kill C. elegans through the production of hydrogen peroxide, and because long-lived C. elegans daf-2 and age-1 mutants are more resistant to oxidative stress, Bolm et al. suggest that the apparent resistance of these mutants to bacterial pathogens is a consequence of their tolerance to reactive oxygen species.

Bolm M et al. (2004) Science "Bacterial resistance in daf-2 mutants."

Jansen WTM, Chhatwal GS, Bolm M

[Science, 2004]

In their Brevia "Long-lived C. elegans daf-2 mutants are resistant to bacterial pathogens," D.A. Garsin et al. show that long-lived C. elegans daf-2 mutants are resistant to killing by bacterial pathogens. Partial loss-of-function mutations in daf-2, which encodes an insulin-like receptor, results in de-repression of the transcription factor daf-16, leading to life extension and increased resistance to bacterial pathogens Enterococcus faecalis, Staphylococcus aureus, and Pseudomonas aeruginosa.

Segalat L (2004) Neuromuscul Disord "Reply to de Luca: Prednisone in dystrophin-deficient Caenorhabditis elegans."

Segalat L

[Neuromuscul Disord, 2004]

In her commentary on our recently published paper, A. de Luca questions the approach consisting in screening random molecules on a dystrophin-deficient invertebrate model (C. elegans) in order to identify potential therapeutic clues.

Silverman PH (1999) Science "C. elegans as a model."

Silverman PH

[Science, 1999]

Elizabeth Pennisi, in her excellent commentary "Worming secrets from the C. elegans" (News Focus, 11 Dec 1998, p.1972), states that "The first person to sense that the worm might take on such a prominent role in biology was molecular biologist Sydney Brenner." I am sure that Brenner would wish to acknowledge the role that Ellsworth C. Dougherty played in this matter. Dougherty originally described in 1949, "[a] new species of the free-living nematode genus Rhabditis of interest in comparative physiology and genetics".

Chalfie M et al. (1993) Nature "Degenerin similarities."

Chalfie M, Driscoll MA, Huang MX

[Nature, 1993]

We were delighted to hear, before publication on 4 February, that Canessa et al. had identified a gene whose product, arEnaC conveys amiloride sensitivity on Xenopus oocytes and exhibits extensive similarity to two Caenorhabditis elegans genes, deg-1 and emc-4, that can mutate to produce neuronal degeneration. We have called the products of these C. elegans genes degenerins. Here we would like to point out that the similarity extends from our previously published sequences, demonstrating that the mammalian and C. elegans genes are members of the same gene family.

Mounsey A et al. (2002) Genome Res "Evidence suggesting that a fifth of annotated Caenorhabditis elegans genes may be pseudogenes."

Mounsey A, Bauer P, Hope IA

[Genome Res, 2002]

Only a minority of the genes, identified in the Caenorhabditis elegans genome sequence data by computer analysis, have been characterized experimentally. We attempted to determine the expression patterns for a random sample of the annotated genes using reporter gene fusions. A low success rate was obtained for evolutionarily recently duplicated genes. Analysis of the data suggests that this is not due to conditional or low-level expression. The remaining explanation is that most of the annotated genes in the recently duplicated category are pseudogenes, a proportion corresponding to 20% of all of the annotated C elegans genes. Further Support for this Surprisingly high figure was sought by comparing sequences for families of recently duplicated C elegans genes. Although only a preliminary analysis, clear evidence for a gene having been recently inactivated by genetic drift was found for many genes in the recently duplicated category. At least 4% of the annotated C elegans genes call be recognized as pseudogenes simply from closer inspection of the sequence data. Lessons learned in identifying pseudogenes in C elegans could be of value in the annotation of the genomes of other species where, although there may be fewer pseudogenes, they may be harder to detect.