WormBase: a comprehensive resource for nematode research

Harris, Todd W.; Antoshechkin, Igor; Bieri, Tamberlyn; Blasiar, Darin; Chan, Juancarlos; Chen, Wen J.; Cruz, Norie De La; Davis, Paul A.; Duesbury, Margaret; Fang, Ruihua; Fernandes, Jolene S.; Han, Michael; Kishore, Ranjana; Lee, Raymond Y. N.; Müller, Hans‐Michael; Nakamura, Cecilia; Ozersky, Philip; Petcherski, Andrei; Rangarajan, Arun; Rogers, Anthony; Schindelman, Gary; Schwarz, Erich M.; Tuli, Mary Ann; Auken, Kimberly Van; Wang, Daniel; Wang, Xiaodong; Williams, Gary W.; Yook, Karen; Durbin, Richard; Stein, Lincoln; Strouboulis, John; Sternberg, Paul W.

doi:10.1093/nar/gkp952

Cited by 343 publications

(355 citation statements)

References 21 publications

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“…c Data from microarray studies as reported in WormBase (Harris et al 2010). d The fecundity 6 SEM of hc198; spe-27 mutant worms transformed with the wild-type copy of the gene.…”

Section: Resultsmentioning

confidence: 99%

A New Player in the Spermiogenesis Pathway of Caenorhabditis elegans

et al. 2015

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Precise timing of sperm activation ensures the greatest likelihood of fertilization. Precision in Caenorhabditis elegans sperm activation is ensured by external signaling, which induces the spherical spermatid to reorganize and extend a pseudopod for motility. Spermatid activation, also called spermiogenesis, is prevented from occurring prematurely by the activity of SPE-6 and perhaps other proteins, termed "the brake model." Here, we identify the spe-47 gene from the hc198 mutation that causes premature spermiogenesis. The mutation was isolated in a suppressor screen of spe-27(it132ts), which normally renders worms sterile, due to defective transduction of the activation signal. In a spe-27(+) background, spe-47(hc198) causes a temperature-sensitive reduction of fertility, and in addition to premature spermiogenesis, many mutant sperm fail to activate altogether. The hc198 mutation is semidominant, inducing a more severe loss of fertility than do null alleles generated by CRISPR-associated protein 9 (Cas9) technology. The hc198 mutation affects an major sperm protein (MSP) domain, altering a conserved amino acid residue in a b-strand that mediates MSP-MSP dimerization. Both N-and C-terminal SPE-47 reporters associate with the forming fibrous body (FB)-membranous organelle, a specialized sperm organelle that packages MSP and other components during spermatogenesis. Once the FB is fully formed, the SPE-47 reporters dissociate and disappear. SPE-47 reporter localization is not altered by either the hc198 mutation or a C-terminal truncation deleting the MSP domain. The disappearance of SPE-47 reporters prior to the formation of spermatids requires a reevaluation of the brake model for prevention of premature spermatid activation.

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“…c Data from microarray studies as reported in WormBase (Harris et al 2010). d The fecundity 6 SEM of hc198; spe-27 mutant worms transformed with the wild-type copy of the gene.…”

Section: Resultsmentioning

confidence: 99%

A New Player in the Spermiogenesis Pathway of Caenorhabditis elegans

et al. 2015

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“…(A) Scale drawing of UNC--16 showing the location of nonsense mutations isolated in this study, conserved regions, and regions known to interact with other proteins from previous studies of UNC--16 and its JIP3 orthologs. Percentages refer to percent identities when comparing the indicated regions of UNC--16 (ZK1098.10b.1 from www.wormbase.org; freeze WS200; (HARRIS et al 2009) to its human JIP3 ortholog (NP_003962). References for interaction sites are as follows: KHC (Kinesin Heavy Chain) ; JNK (c--Jun N--terminal kinase) , KLC (Kinesin Light Chain) .…”

Section: Figure S1mentioning

confidence: 99%

An Organelle Gatekeeper Function forCaenorhabditis elegansUNC-16 (JIP3) at the Axon Initial Segment

et al. 2013

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Neurons must cope with extreme membrane trafficking demands to produce axons with organelle compositions that differ dramatically from those of the cell soma and dendrites; however, the mechanism by which they accomplish this is not understood. Here we use electron microscopy and quantitative imaging of tagged organelles to show that Caenorhabditis elegans axons lacking UNC-16 (JIP3/Sunday Driver) accumulate Golgi, endosomes, and lysosomes at levels up to 10-fold higher than wild type, while ER membranes are largely unaffected. Time lapse microscopy of tagged lysosomes in living animals and an analysis of lysosome distributions in various regions of unc-16 mutant axons revealed that UNC-16 inhibits organelles from escaping the axon initial segment (AIS) and moving to the distal synaptic part of the axon. Immunostaining of native UNC-16 in C. elegans neurons revealed a localized concentration of UNC-16 at the initial segment, although UNC-16 is also sparsely distributed in distal regions of axons, including the synaptic region. Organelles that escape the AIS in unc-16 mutants show bidirectional active transport within the axon commissure that occasionally deposits them in the synaptic region, where their mobility decreases and they accumulate. These results argue against the long-standing, untested hypothesis that JIP3/Sunday Driver promotes anterograde organelle transport in axons and instead suggest an organelle gatekeeper model in which UNC-16 (JIP3/Sunday Driver) selectively inhibits the escape of Golgi and endosomal organelles from the AIS. This is the first evidence for an organelle gatekeeper function at the AIS, which could provide a regulatory node for controlling axon organelle composition. NEURONS have a unique cell biology that presents daunting membrane trafficking challenges. For example, they must selectively transport two classes of regulated secretory vesicles (synaptic vesicles and dense core vesicles) long distances into axons, but only after the vesicles have completed their maturation process in the cell soma, during which they arise from, and interact with, other organelles in the soma. Neurons must also restrict, or even prevent, the flow of some organelles, such as Golgi, lysosomes, and endosomes, into the distal synaptic region of axons, which are relatively devoid of these organelles compared to cell somas.However, under special conditions, such as the need for axon repair or growth, neurons may require these organelles in axons. The potential hazards of excessive organelle transport into axons may include organelle traffic jams within narrow axons, reduced synaptic vesicle production as synaptic vesicle proteins are transported away from the cell soma before they are assembled into mature vesicles, and the disruption of membrane trafficking pathways in the synaptic region of axons caused by the inappropriate presence of cell soma organelles.A crucial regulatory domain for controlling axon composition is the region at or near the junction of the cell soma and axon, designated th...

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“…Next, we compared the list of signalogs and their predicted pathway memberships to pathway annotations found in pathway databases, as well as the list of ortholog predictions to previously published interolog predictions. To assess the novelty of signalogs and quantify the confidence level of each prediction, we performed semiautomated searches using PubMed, UniProt, GO, Wormbase, FlyBase, iHOP, and Chilibot web services [15,18,[29][30][31][32]. During this process, direct manual curation and Python scripts checking multiple proteins in one webservice were used.…”

Section: Defining the Novelty Of Signaling Protein Predictions Basedmentioning

confidence: 99%

Uniform Curation Protocol of Metazoan Signaling Pathways to Predict Novel Signaling Components

Pálfy

Farkas

Vellai

et al. 2013

Methods in Molecular Biology

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A relatively large number of signaling databases available today have strongly contributed to our understanding of signaling pathway properties. However, pathway comparisons both within and across databases are currently severely hampered by the large variety of data sources and the different levels of detail of their information content (on proteins and interactions). In this chapter, we present a protocol for a uniform curation method of signaling pathways, which intends to overcome this insufficiency. This uniformly curated database called SignaLink (http://signalink.org) allows us to systematically transfer pathway annotations between different species, based on orthology, and thereby to predict novel signaling pathway components. Thus, this method enables the compilation of a comprehensive signaling map of a given species and identification of new potential drug targets in humans.We strongly believe that the strict curation protocol we have established to compile a signaling pathway database can also be applied for the compilation of other (e.g., metabolic) databases. Similarly, the detailed guide to the orthology-based prediction of novel signaling components across species may also be utilized for predicting components of other biological processes.

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WormBase: a comprehensive resource for nematode research

Cited by 343 publications

References 21 publications

A New Player in the Spermiogenesis Pathway of Caenorhabditis elegans

A New Player in the Spermiogenesis Pathway of Caenorhabditis elegans

An Organelle Gatekeeper Function forCaenorhabditis elegansUNC-16 (JIP3) at the Axon Initial Segment

Uniform Curation Protocol of Metazoan Signaling Pathways to Predict Novel Signaling Components

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