Westlund B et al. (1997) Advances in Developmental Biology "Regulation of germline proliferation in Caenorhabditis elegans."

Wilson Berry L, Westlund B, Schedl TB

[Advances in Developmental Biology, 1997]

Germline development is unique within Caenorhabditis elegans for a number of reasons. First, the germline is the only organ whose cells undergo meiotic development. Second, in contrast to the essentially invariant cell lineages of the C. elegans soma, germ cells divide a variable number of times. Finally, a subset of germ cells remain in a mitotic, undifferentiated state throughout the lifetime of the animal:: they serve as a stem cell population for the germ line. Thus, one important decision germ cells face is whether to remain mitotic or enter meiotic prophase. A large body of work has focused on elucidating the molecular mechanism underlying this process. Taken together, these data demonstrate that the GLP-1 signaling pathway is crucial for the mitosis verses meiosis decision. Here we discuss in detail what is known about this pathway in the C. elegans germ line. Since GLP-1 is a Notch homolog and the Notch signaling pathway appears to be conserved from nematodes to mammals, we also summarize some of the findings that have come from studies on other Notch family members, their ligands, and downstream effectors. In addition, several genes have been characterized that do not appear to be involved directly in the mitosis verses meiosis decision, but when mutated display ectopic proliferation or reduced proliferation defects. We describe their mutant phenotypes as well as any known interactions with glp-1.

Schierenberg E et al. (1992) Seminars in Developmental Biology "The establishment of embryonic axes and determination of cell fates in embryos of the nematode Caenorhabditis elegans."

Schierenberg E, Strome S

[Seminars in Developmental Biology, 1992]

At the 4-cell stage of the C. elegans embryo, three axes can be defined: anterior-posterior (A-P), dorsal-ventral (D-V), and left-right (L-R). The A-P axis first becomes obvious in the newly fertilized 1-cell embryo. Pronouned cytoplasmic assymmetries arise along the A-P axis during the first cell cycle, after which the zygote undergoes a series of stem cell-like cleavages with an A-P orientation of the mitotic spindle; these cleavages generate several somatic founder cells and a primordial germ cell. The D-V and L-R axes are defined by the direction of spindle rotation as the 2-cell embryo divides into four cells. In contrast to the A-P axis, there do not appear to be cellular asymmetries associated with the D-V and L-R axes, and both axes can easily be reversed by micromanipulation. Thus, with respect to the roles that the embryonic axes serve in cell-fate determination in the early C. elegans embryo, it appears that internally transmitted developmental information is differentially segregated along the A-P axis, but not along the D-V or L-R axes. Instead, D-V and L-R differences in the fates of cells within lineages appear to be dictated by differential

Favello A et al. (1995) Methods Cell Biol "Genomic DNA sequencing methods."

Wilson RK, Hillier L, Favello A

[Methods Cell Biol, 1995]

Sequence analysis of cosmids from C. elegans and other organisms currently is best done using the random or "shotgun" strategy (Wilson et al., 1994). After shearing by sonication, DNA is used to prepare M13 subclone libraries which provide good coverage and high-quality sequence data. The subclones are assembled and the data edited using software tools developed especially for C. elegans genomic sequencing. These same tools facilitate much of the subsequent work to complete both strands of the sequence and resolve any remaining ambiguities. Analysis of the finished sequence is then accomplished using several additional computer tools including Genefinder and ACeDB. Taken together, these methods and tools provide a powerful means for genome analysis in the nematode.

Best AM et al. (2018) Cell Microbiol "Evasion of phagotrophic predation by protist hosts and innate immunity of metazoan hosts by Legionella pneumophilla."

Best AM, Kwaik YA

[Cell Microbiol, 2018]

Legionella pneumophila is a ubiquitous environmental bacterium that has evolved to infect and proliferate within amoebae and other protists. It is thought that accidental inhalation of contaminated water particles by humans is what has enabled this pathogen to proliferate within alveolar macrophages and cause pneumonia. However, the highly evolved macrophages are equipped more sophisticated innate defense mechanisms than protists, such as the evolution of phagotrophic feeding into phagocytosis with more evolved innate defense processes. Not surprisingly, the majority of proteins involved in phagosome biogenesis (~80%) have origins in the phagotrophy stage of evolution. There are a plethora of highly evolved cellular and innate metazoan processes, not represented in Protist biology, that are modulated by L. pneumophila; including TLR2 signaling, NF-B, apoptotic and inflammatory processes, histone modification, caspases, and the NLRC-Naip5 inflammasomes. Importantly, L. pneumophila infects hemocytes of the invertebrate Galleria mellonella, kill G. mellonella larvae, and proliferate in and kill Drosophila adult flies and Caenorhabditis elegans. Although co-evolution with protist hosts has provided a substantial blueprint for L. pneumophila to infect macrophages, we discuss the further evolutionary aspects of co-evolution of L. pneumophila and its adaptation to modulate various highly evolved innate metazoan processes prior to becoming a human pathogen.

Li R et al. (2021) Food Funct "Small berries as health-promoting ingredients: a review on anti-aging effects and mechanisms in Caenorhabditis elegans."

Pan S, Li R, Xu T, Tao M, Xu X, Wu T

[Food Funct, 2021]

Aging is an inevitable, irreversible, and complex process of damage accumulation and functional decline, increasing the risk of various chronic diseases. However, for now no drug can delay aging process nor cure aging-related diseases. Nutritional intervention is considered as a key and effective strategy to promote healthy aging and improve life quality. Small berries, as one of the most common and popular fruits, have been demonstrated to improve cognitive function and possess neuroprotective activities. However, the anti-aging effects of small berries have not been systematically elucidated yet. This review mainly focuses on small berries' anti-aging activity studies involving small berry types, active components, the utilized model organism <i>Caenorhabditis elegans</i> (<i>C. elegans</i>), related signaling pathways, and molecular mechanisms. The purpose of this review is to propose effective strategies to evaluate the anti-aging effects of small berries and provide guidance for the development of anti-aging supplements from small berries.

Lee SK et al. (2013) Int J Biochem Cell Biol "Dicarbonyl/l-xylulose reductase (DCXR): The multifunctional pentosuria enzyme."

Ahnn J, Lee SK, Son LT, Choi HJ

[Int J Biochem Cell Biol, 2013]

Dicarbonyl/L-xylulose reductase (DCXR) is a highly conserved and phylogenetically widespread enzyme converting L-xylulose into xylitol. It also reduces highly reactive -dicarbonyl compounds, thus performing a dual role in carbohydrate metabolism and detoxification. Enzymatic properties of DCXR from yeast, fungi and mammalian tissue extracts are extensively studied. Deficiency of the DCXR gene causes a human clinical condition called pentosuria and low DCXR activity is implicated in age-related diseases including cancers, diabetes, and human male infertility. While mice provide a model to study clinical condition of these diseases, it is necessary to adopt a physiologically tractable model in which genetic manipulations can be readily achieved to allow the fast genetic analysis of an enzyme with multiple biological roles. Caenorhabditis elegans has been successfully utilized as a model to study DCXR. Here, we discuss the biochemical properties and significance of DCXR activity in various human diseases, and the utility of C. elegans as a research platform to investigate the molecular and cellular mechanism of the DCXR biology.

Reed E et al. (2018) J Neurochem "Animal models of Wilson disease."

Lutsenko S, Bandmann O, Reed E

[J Neurochem, 2018]

Wilson disease (WD) is an autosomal recessive disorder of copper metabolism manifesting with hepatic, neurological and psychiatric symptoms. The limitations of the currently available therapy for WD (particularly in the management of neuropsychiatric disease), together with our limited understanding of key aspects of this illness (e.g. neurological vs hepatic presentation) justify the ongoing need to study WD in suitable animal models. Four animal models of WD have been established: the Long-Evans Cinnamon rat, the toxic-milk mouse, the Atp7b knockout mouse and the Labrador retriever. The existing models of WD all show good similarity to human hepatic WD and have been helpful in developing an improved understanding of the human disease. As mammals, the mouse, rat and canine models also benefit from high homology to the human genome. However, important differences exist between these mammalian models and human disease, particularly the absence of a convincing neurological phenotype. This review will first provide an overview of our current knowledge of the orthologous genes encoding ATP7B and the closely related ATP7A protein in C. elegans, Drosophila and zebrafish (Danio rerio) and then summarise key characteristics of rodent and larger mammalian models of ATP7B-deficiency. This article is protected by copyright. All rights reserved.

Cerpa W et al. (2005) Mol Aspects Med "Is there a role for copper in neurodegenerative diseases?"

Cerpa W, Inestrosa NC, Varela-Nallar L, Minniti AN, Reyes AE

[Mol Aspects Med, 2005]

Copper is an essential metal in living organisms; thus, the maintenance of adequate copper levels is of vital importance and is highly regulated. Dysfunction of copper metabolism leading to its excess or deficiency results in severe ailments. Two examples of illnesses related to alterations in copper metabolism are Menkes and Wilson diseases. Several proteins are involved in the maintenance of copper homeostasis, including copper transporters and metal chaperones. In the last several years, the beta-amyloid-precursor protein (beta-APP) and the prion protein (PrP(C)), which are related to the neurodegenerative disorders Alzheimer and prion diseases respectively, have been associated with copper metabolism. Both proteins bind copper through copper-binding domains that also have been shown to reduce copper in vitro. Moreover, this ability to reduce copper is associated with a neuroprotective effect exerted by the copper-binding domain of both proteins against copper in vivo. In addition to a functional link between copper and beta-APP or PrP(C), evidence suggests that copper has a role in Alzheimer and prion diseases. Here, we review the evidence that supports both, the role of beta-APP and PrP(C), in copper metabolism and the putative role of copper in neurodegenerative diseases.

Emmons SW (1987) Cell "Mechanisms of C. elegans development."

Emmons SW

[Cell, 1987]

What are the respective roles in multicellular development of mechansims acting at the level of the cell and mechanisms acting at the level of the cell group? It's an old question, and one that is central to the problem of developmental biology. Even early in this century it had long been debated "whether the character of growth and morphogenesis is a cause or a result of the corresponding activities on the part of the component cells individually considered" (E.B. Wilson, The Cell in Development and Heredity, Macmillan, 1925, p. 1029). The question is now being reexamined in the nematode Caenorhabditis elegans, an organism whose embryonic and postembryonic development are easily observed. Initial studies emphasized the reproducibility and, thus, the apparent cell-autonomy of development in the animal. Little flexibility in cell division patterns or differentiation was found in blastomere isolation experiments or after microsurgery with a laser beam. More recent results, however, demonstrate that cellular interactions are more important. These new results, combined with new molecular techniques that make it possible to isolate genes defined by mutations and to reintroduce cloned genes into the germ line, open the way to a molecular analysis of developmental mechanisms that are likely to be widespread in the animal kingdom.

Lv Z et al. (2015) Parasitol Res "Genome mining offers a new starting point for parasitology research."

Wu Z, Ji P, Li H, Cai Y, Zhang L, Luo S, Wang H, Lv Z

[Parasitol Res, 2015]

Parasites including helminthes, protozoa, and medical arthropod vectors are a major cause of global infectious diseases, affecting one-sixth of the world's population, which are responsible for enormous levels of morbidity and mortality important and remain impediments to economic development especially in tropical countries. Prevalent drug resistance, lack of highly effective and practical vaccines, as well as specific and sensitive diagnostic markers are proving to be challenging problems in parasitic disease control in most parts of the world. The impressive progress recently made in genome-wide analysis of parasites of medical importance, including trematodes of Clonorchis sinensis, Opisthorchis viverrini, Schistosoma haematobium, S. japonicum, and S. mansoni; nematodes of Brugia malayi, Loa loa, Necator americanus, Trichinella spiralis, and Trichuris suis; cestodes of Echinococcus granulosus, E. multilocularis, and Taenia solium; protozoa of Babesia bovis, B. microti, Cryptosporidium hominis, Eimeria falciformis, E. histolytica, Giardia intestinalis, Leishmania braziliensis, L. donovani, L. major, Plasmodium falciparum, P. vivax, Trichomonas vaginalis, Trypanosoma brucei and T. cruzi; and medical arthropod vectors of Aedes aegypti, Anopheles darlingi, A. sinensis, and Culex quinquefasciatus, have been systematically covered in this review for a comprehensive understanding of the genetic information contained in nuclear, mitochondrial, kinetoplast, plastid, or endosymbiotic bacterial genomes of parasites, further valuable insight into parasite-host interactions and development of promising novel drug and vaccine candidates and preferable diagnostic tools, thereby underpinning the prevention and control of parasitic diseases.