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[
WormBook,
2009]
Autophagy is a ubiquitous cellular process responsible for the bulk degradation of cytoplasmic components through an autophagosomal-lysosomal pathway. Genetic screens, primarily in S. cerevisiae, have identified numerous genes that are essential for autophagy. Many of these genes have orthologs in higher eukaryotes, including C. elegans, Drosophila, and mammals. Gene knockdown/knockout studies in C. elegans have been useful to probe the functions of autophagy in an intact multicellular organism that undergoes development to produce different cell types. This review summarizes important themes that have emerged regarding the roles of autophagy in C. elegans in adaptation to stress, aging, normal reproductive growth, cell death, cell growth control, neural synaptic clustering, and the degradation of aggregate-prone proteins.
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[
Adv Exp Med Biol,
2010]
Aging is a process in which individuals undergo an exponential decline in vitality, leading to death. In the last two decades, the study of the molecular regulation of aging in model organisms, particularly in C. elegans, has greatly expanded our knowledge of aging. Multiple longevity pathways, such as insulin-like growth factor signaling, TOR signaling, dietary restriction and mitochondrial activity, control aging in C. elegans. Recent genetic studies indicate that autophagy, an evolutionary conserved lysosomal degradation pathway, interacts with various longevity signals in the regulation of C. elegans life span. Here, we review the current progress in understanding the role of autophagy in the regulation of C. elegans life span.
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[
Curr Biol,
2005]
Aurora B kinases play important roles during mitosis in eukaryotic cells; new work in Caenorhabditis elegans has identified the Tousled kinase TLK-1 as a substrate activator of the model nematode''''s Aurora B kinase AIR-2 which acts to ensure proper chromosome segregation during
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[
Genetics,
2019]
The <b>T</b>arget <b>o</b>f <b>R</b>apamycin (TOR or mTOR) is a serine/threonine kinase that regulates growth, development, and behaviors by modulating protein synthesis, autophagy, and multiple other cellular processes in response to changes in nutrients and other cues. Over recent years, TOR has been studied intensively in mammalian cell culture and genetic systems because of its importance in growth, metabolism, cancer, and aging. Through its advantages for unbiased, and high-throughput, genetic and <i>in vivo</i> studies, <i>Caenorhabditis elegans</i> has made major contributions to our understanding of TOR biology. Genetic analyses in the worm have revealed unexpected aspects of TOR functions and regulation, and have the potential to further expand our understanding of how growth and metabolic regulation influence development. In the aging field, <i>C. elegans</i> has played a leading role in revealing the promise of TOR inhibition as a strategy for extending life span, and identifying mechanisms that function upstream and downstream of TOR to influence aging. Here, we review the state of the TOR field in <i>C. elegans</i>, and focus on what we have learned about its functions in development, metabolism, and aging. We discuss knowledge gaps, including the potential pitfalls in translating findings back and forth across organisms, but also describe how TOR is important for <i>C. elegans</i> biology, and how <i>C. elegans</i> work has developed paradigms of great importance for the broader TOR field.
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[
Trends in Cell Biology,
1996]
Cellular microtubules assemble and disassemble at a variety of rates and frequencies, and these properties contribute directly to the cell-cycle-associated rearrangements of the microtubule cytoskeleton and to the molecular basis of mitosis. The kinetics of assembly/disassembly are governed, in part, by the hydrolysis of GTP bound to the B-tubulin nucleotide-binding site. The B-tubulin GTP-binding site, therefore, lies at the heart of microtubule assembly-disassembly kinetics, and the elucidation of its structure is central to an understanding of the cellular behaviour of microtubules. Unfortunately, the crystallographic structure of B-tubulin is not yet available. In this review, we describe the progress being made using mutagenesis and biochemical studies to understand the structure of this unusual GTP-binding site.
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J Exp Zool,
1999]
A memorable workshop, focused on causal mechanisms in metazoan evolution and sponsored by NASA, was held in early June 1998, at MBL. The workshop was organized by Mike Levine and Eric H. Davidson, and it included the PI and associates from 12 different laboratories, a total of about 30 people. Each laboratory had about two and one half hours in which to represent its recent research and cast up its current ideas for an often intense discussion. In the following we have tried to enunciate some of the major themes that emerged, and to reflect on their implications. The opinions voiced are our own. We would like to tender apologies over those contributions we have not been able to include, but this is not, strictly speaking, a meeting review. Rather we have focused on those topics that bear more directly on evolutionary mechanisms, and have therefore slighted some presentations (including some of our own), that were oriented mainly toward developmental processes. J. Exp. Zool. (Mol. Dev. Evol. ) 285:104-115, 1999.
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[
Microbiol Mol Biol Rev,
2021]
SUMMARYExtensive use of chemical insecticides adversely affects both environment and human health. One of the most popular biological pest control alternatives is bioinsecticides based on <i>Bacillus thuringiensis</i> This entomopathogenic bacterium produces different protein types which are toxic to several insect, mite, and nematode species. Currently, insecticidal proteins belonging to the Cry and Vip3 groups are widely used to control insect pests both in formulated sprays and in transgenic crops. However, the benefits of <i>B. thuringiensis</i>-based products are threatened by insect resistance evolution. Numerous studies have highlighted that mutations in genes coding for surrogate receptors are responsible for conferring resistance to <i>B. thuringiensis</i> Nevertheless, other mechanisms may also contribute to the reduction of the effectiveness of <i>B. thuringiensis</i>-based products for managing insect pests and even to the acquisition of resistance. Here, we review the relevant literature reporting how invertebrates (mainly insects and <i>Caenorhabditis elegans</i>) respond to exposure to <i>B. thuringiensis</i> as either whole bacteria, spores, and/or its pesticidal proteins.
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[
1986]
Wild-type body wall muscle cells of Caenorhabditis elegans produce at a constant ratio two myosin heavy chain isoforms, A and B, that form homodimeric myosins. Electron microscopy of negatively stained complexes of isoform-specific antibodies with isolated thick filaments shows that the surface of the 9.7 =B5m long filament is differentiated with respect to myosin content: a medial 1.8 =B5m zone contains myosin A and two polar 4.4 = =B5m zones contain myosin B. Biochemical and electron microscopic studies show that at 0.45 M KC1, pH 6.35, myosin B and paramyosin are solubilized. The medial all-myosin A region with novel core structures extending in a polar manner remain. These dissociation experiments suggest a sequential model for wild-type thick filament assembly in which myosins A and B would participate in the initiation and termination of assembly, respectively. Analysis of mutant thick filaments clarifies the relationship of the myosin isoforms. CB190 (
unc-54 I) thick filaments contain myosin A only and have normal length. CB1214 (
unc-15 I) mutants produce no paramyosin, and their thick filaments are composed of a medial myosin region
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[
Results Probl Cell Differ,
2017]
Asymmetric cell division is a common mode of cell differentiation during the invariant lineage of the nematode, C. elegans. Beginning at the four-cell stage, and continuing throughout embryogenesis and larval development, mother cells are polarized by Wnt ligands, causing an asymmetric inheritance of key members of a Wnt/B-catenin signal transduction pathway termed the Wnt/B-catenin asymmetry pathway. The resulting daughter cells are distinct at birth with one daughter cell activating Wnt target gene expression via B-catenin activation of TCF, while the other daughter displays transcriptional repression of these target genes. Here, we seek to review the body of evidence underlying a unified model for Wnt-driven asymmetric cell division in C. elegans, identify global themes that occur during asymmetric cell division, as well as highlight tissue-specific variations. We also discuss outstanding questions that remain unanswered regarding this intriguing mode of asymmetric cell division.
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[
Ciba Found Symp,
1987]
Human lymphatic filariasis is caused mainly by Wuchereria bancrofti, Brugia malayi and Brugia timori. Of the estimated 90.2 million people infected, more than 90% have bancroftian and less than 10% brugian filariasis. The distribution and transmission of the disease are closely associated with socioeconomic and behavioural factors in endemic populations. Urban W. bancrofti infection, as seen in South-East Asia, is related to poor urban sanitation, which leads to intense breeding of Culex quiquefasciatus, the principal vector. Rural strains of W. bancrofti are transmitted primarily by Anopheles spp. and Aedes spp. mosquitoes. Brugian filariasis is mainly a rural disease transmitted by Mansonia, Anopheles and Aedes spp. mosquitoes. The periodic form of B. malayi is principally a human parasite, whereas the subperiodic form is zoonotically transmitted in some countries. The control of filariasis has relied on chemotherapy, vector control and reduction of human-vector contact. Although eradication of W. bancrofti and periodic B. malayi can be achieved, it is possible only to reduce transmission of zoonotic subperiodic B. malayi in some areas. A rational approach to control should consider ecological, socioeconomic and behavioural factors and, where feasible, integrate control programmes into the delivery system for primary health care.