Benny H H Cheung et al. (2002) European Worm Meeting "Genes regulating social feeding behaviour in C. elegans."

Benny H H Cheung, Mario De Bono

[European Worm Meeting, 2002]

Natural isolates of C. elegans exhibit either social or solitary feeding behaviour1,2,3,4. Social strains aggregate and feed together on a bacterial lawn; solitary strains show no aggregation and feed in isolation. This variation is associated with a single amino acid change in NPR-1, a seven transmembrane receptor related to mammalian neuropeptide Y receptors. Null mutations in npr-1 transform solitary wild strains into strongly social animals.

Benny H H Cheung et al. (2001) International C. elegans Meeting "Genes regulating social feeding behaviour in C elegans."

Benny H H Cheung, Mario De Bono

[International C. elegans Meeting, 2001]

Natural isolates of C. elegans exhibit either social or solitary feeding behaviour. Social strains aggregate and feed together on a bacterial lawn; solitary strains show no aggregation and feed in isolation. This variation is due to a single amino acid change in NPR-1, a seven transmembrane receptor related to mammalian neuropeptide Y receptors. Null mutations in npr-1 transform solitary wild strains into strongly social animals. We wish to elucidate the molecular pathways controlling social versus solitary feeding. Two EMS mutagenesis screens have been performed, starting with strongly social npr-1 (null) animals in both N2 and CB4856 (a snip-SNP-bearing strain) backgrounds, and selecting for mutants that feed alone. About sixty mutations have been isolated thus far, which show varying degrees of suppression of social behaviour. Several known suppressors (e.g. odr-8 , osm-9 etc.), which function in other sensory pathways, have been pulled out from these two screens. Fifteen strong, novel suppressors have been chosen, mapped and characterised further. We hope these suppressors will identify molecules that either regulate the choice between social and solitary feeding, or are essential signal transduction components of the sensory inputs leading to social behaviour. Davis M.W. and Avery L.. Social Behavior in bor-1 Mutants Depends on Bacterial Smell. Worm Breeder's Gazette 11(5): 69. Cassada R.. Burrowing, Spontaneous Mutants, etc. with Another Wildtype Strain. Worm Breeder's Gazette 9(3): 29. Hodgkin J. and Doniach T. (1997). Natural variation and copulatory plug formation in Caenorhabditis elegans . Genetics 146: 149-164. de Bono M. and Bargmann C.I. (1998). Natural variation in a neuropeptide Y receptor homolog modifies social behavior and food response in C. elegans . Cell 94: 679-689.

Hutter H (2012) Worm "Introducing Worm: The journal."

Hutter H

[Worm, 2012]

Ryan, Veronica H. et al. MicroPubl Biol

Ryan, Veronica H., Hart, Anne C.

[MicroPubl Biol, 2021]

Although some RNA-binding proteins are known to contribute to neurodegeneration, the genetic interaction between the genes encoding these proteins is unclear. Here, we examine the interaction between sym-2, the gene encoding an ortholog of hnRNPF and hnRNPH, and hrpa-1, the ortholog of of the gene encoding hnRNPA2, which when mutated causes multisystem proteinopathy. We find that after 22 hours, but not 4 hours, of paraquat-induced oxidative stress, sym-2(mn617) has a mild glutamatergic neurodegeneration phenotype. Interestingly, this defect is rescued by expression of chimeric WT hrpa-1, but not mutant. Thus, we identify a curious genetic interaction between sym-2 and hrpa-1.

Hall David H et al. (2008) "C. elegans Atlas"

Altun Zeynep F, Hall David H

[2008]

Tabara H (2001) Tanpakushitsu Kakusan Koso "[RNAi and PTGS in eukaryotes]"

Tabara H

[Tanpakushitsu Kakusan Koso, 2001]

Nishimura H et al. (2017) Curr Biol "Spermatogenesis."

L'Hernault SW, Nishimura H

[Curr Biol, 2017]

Most organisms consist of two cell lineages - somatic cells and germ cells. The former are required for the current generation, and the latter create offspring. Male and female germ cells are usually produced during spermatogenesis and oogenesis, which take place in the testis and the ovary, respectively. Spermatogenesis involves the differentiation of spermatogonial stem cells into spermatocytes via mitotic cell division and the production of haploid spermatids from the tetraploid primary spermatocytes via meiotic cell division. Spermatids subsequently give rise to spermatozoa in the final phase of spermatogenesis, called spermiogenesis. These fundamental steps, where mitotic proliferation precedes meiosis during spermatogenesis, are observed in a wide variety of organisms. However, developing a comprehensive understanding of the cell biology and genetics of spermatogenesis is difficult for most species because it occurs within a complex testicular environment characterized by the intimate association of developing sperm with accessory cells. In this Primer, we summarize the processes of spermatogenesis occurring in two pivotal model animals - mouse and Caenorhabditis elegans - and compare them to consider which important features might be evolutionarily conserved.

Puccio H (2009) J Neurol "Multicellular models of Friedreich ataxia."

Puccio H

[J Neurol, 2009]

Patients with Friedreich ataxia (FRDA) have severely reduced levels of the mitochondrial protein frataxin, which results from a large GAA triplet-repeat expansion within the frataxin gene (FXN). High evolutionary conservation of frataxin across species has enabled the development of disease models of FRDA in various unicellular and multicellular organisms. Mouse models include classical knockout models, in which the Fxn gene is constitutively inactivated, and knock-in models, in which a GAA repeat mutation or the conditional allele is inserted into the genome. Recently, "humanised" GAA repeat expansion mouse models were obtained by combining the constitutive knockout with the transgenic expression of a yeast artificial chromosome carrying the human FRDA locus. In lower organisms such as Caenorhabditis elegans and Drosophila, straight-forward and conditional RNA interference technology has provided an easy way to knock down frataxin expression. Conditional mouse models have been used for pre-clinical trials of potential therapeutic agents, including idebenone, MnTBAP (a superoxide dismutase mimetic), and iron chelators. Various models of FRDA have shown that different, even opposite, phenotypes can be observed, depending on the level of frataxin expression. Additional studies with animal models will be essential for an enhanced understanding of the disease pathophysiology and for the development of better therapies.

Aguilaniu H (2015) Worm "The mysterious relationship between reproduction and longevity."

Aguilaniu H

[Worm, 2015]

A negative correlation between fertility and longevity has been documented in many species under a variety of conditions, but the association is not always observed,(1) leading to heated discussion about the nature of the reproduction-longevity relationship.(2) This debate is further fueled by the fact that no genes or molecules have been clearly shown to link the 2 traits. A recent study by Thondamal etal., in the nematode C. elegans has identified one potential link. The authors showed that the steroid signaling pathway, which regulates reproduction, is activated in response to dietary restriction (DR) and is in fact required for DR-induced lifespan extension.(3) Steroid signaling mutants subjected to DR not only failed to undergo lifespan extension but also exhibited altered germline plasticity. Interestingly, the requirement for steroid signaling was bypassed when germline plasticity was restored, suggesting that the DR response is mediated, at least in part, by signals from the germline. In this commentary, I discuss the implications of these findings. Several theories of aging have proposed the existence of an energetic trade-off between reproduction and lifespan,(4,5) but mechanistic details are lacking. I propose that revisiting and dissecting at the molecular level the link between reproduction, nutrition, and lifespan, will lead to a better understanding of the aging process and its connection to reproduction.

Steller H (1995) Science "Mechanisms and genes of cellular suicide."

Steller H

[Science, 1995]

Apoptosis is a morphologically distinct form of programmed cell death that plays a major role during development, homeostasis, and in many diseases including cancer, acquired immunodeficiency syndrome, and neurodegenerative disorders. Apoptosis occurs through the activation of a cell-intrinsic suicide program. The basic machinery to carry out apoptosis appears to be present in essentially all mammalian cells at all times, but the activation of the suicide program is regulated by many different signals that originate from both the intracellular and the extracellular milieu. Genetic studies in the nematode Caenorhabditis elegans and in the fruit fly Drosophila melanogaster have led to the isolation of genes that are specifically required for the induction of programmed cell death. At least some components of the apoptotic program have been conserved among worms, insects, and vertebrates.