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Curr Biol,
2010]
The protein Lethal giant larvae (LGL) regulates cell polarity in diverse animal models. Now, an LGL orthologue has been identified in the worm Caenorhabditis elegans and is shown to function redundantly with a worm-specific polarity protein, PAR-2.
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[
Elife,
2015]
Chromosome separation is regulated by a cycle that involves a protein undergoing an unusual topological conversion.
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Mol Cell,
2018]
A new mechanism for clearing protein damage from maturing oocytes has been described in a recent study by Bohnert and Kenyon (2017), who demonstrated that sperm-secreted hormones activate a vascular H<sup>+</sup>-ATPase pump that acidifies lysosomes and thus restores protein homeostasis.
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Cell,
2014]
The hexosamine biosynthetic pathway (HBP) generates metabolites for protein N- and O-glycosylation. Wang et al. and Denzel et al. report a hitherto unknown link between the HBP and stress in the endoplasmic reticulum. These studies establish the HBP as a critical component of the cellular machinery of protein homeostasis.
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Nat Genet,
2003]
A new study attempts to amplify and clone all the predicted protein-encoding open reading frames (ORFs) for Caenorhabditis elegans. This analysis confirms many of the predicted genes but suggests roughly 50% of them require correction. Recombining the ORFs into a number of different expression systems can generate functional proteomics kits for characterizing protein activity and interaction networks.
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[
Elife,
2014]
CED-3, a protein that is essential for programmed cell death, also has an unexpected role in the regulation of non-apoptotic genes during normal development.
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[
Nature Immunology,
2004]
The function of the mammalian TIR domain adaptor protein SARM is unclear. In Caenorhabditis elegans, however, the homolog of SARM controls the induction of peptides involved in innate immunity.
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Worm,
2017]
The integrity of the cellular proteome is supported by quality control networks, which govern protein synthesis, folding, and degradation. It is generally accepted that an age-related decline in protein homeostasis (proteostasis) contributes to protein aggregation diseases. However, the mechanistic principles underlying proteostasis imbalance and the impact on life expectancy are not well understood. We recently demonstrated that this interrelation is affected by chaperone-directed ubiquitylation, shifting the amount of the conserved DAF-2/insulin receptor both in Caenorhabditis elegans and Drosophila melanogaster. The ubiquitin ligase CHIP either targets the membrane bound insulin receptor or misfolded proteins for degradation, which depends on the cellular proteostasis status. Increased proteotoxicity triggers chaperone-assisted redirection of CHIP toward protein aggregates, limiting its capacity to degrade the insulin receptor and prevent premature aging. In light of these findings, we discuss a new concept for understanding the impact of proteome imbalance on longevity risk.
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[
Nat Neurosci,
2001]
A characterization of C. elegans lacking the gene for Rim suggests that this protein may be involved in pruning synaptic vesicles for fusion, not in docking or organizing active zones.
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[
Proc Natl Acad Sci U S A,
2003]
The most common neurodegenerative diseases are characterized by the presence of abnormal filamentous protein inclusions in nerve cells of the brain. In Alzheimer's disease, these inclusions are made of hyperphosphorylated tau protein. Together with the extracellular beta-amyloid deposits, they consitute the defining neuropathological characteristics of Alzheimer's disease. Tau inclusions, in the absence of extracellular deposits, are characteristic of progressive supranuclear palsy, corticobasal degeneration, Pick's disease, argyrophilic grain disease, and frontotemporal dementia and parkinsonism linked to chromosome 17. The identification of mutations in Tau in FTDP-17 has established that dysfunction of tau protein is central to the neurodegenerative process. At an experimental level, the expression of mutant human tau in nerve cells is leading to improved models of neurodegeneration. In this issue of PNAS, Kraemer et al. describe lines of Caenorhabditis elegans expressing transgenic wild-type and mutant human tau protein. They represent an important addition to