Functional Properties of the unc-64 Gene Encoding aCaenorhabditis elegans Syntaxin

Ogawa, Hidenori; Harada, Shinichi; Sassa, Toshihiro; Yamamoto, Hiroshi; Hosono, Ryuji

doi:10.1074/jbc.273.4.2192

Cited by 76 publications

(63 citation statements)

References 25 publications

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“…ined the localization of VenusTUNC-6 in the mutants of other exocytosis-related genes, such as snt-1/ synaptotagmin, snb-1/synaptobrevin, unc-64/syntaxin, and unc-13/Munc13 (Maruyama and Brenner 1991;Nonet et al 1993;Nonet et al 1998;Ogawa et al 1998;Saifee et al 1998;Malsam et al 2008; Sü dhof and Rothman 2009). However, the localization of VenusTUNC-6 was not altered in these mutants (Table 2).…”

Section: Resultsmentioning

confidence: 99%

Genes Required for Cellular UNC-6/Netrin Localization in Caenorhabditis elegans

et al. 2010

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UNC-6/Netrin is an evolutionarily conserved, secretory axon guidance molecule. In Caenorhabditis elegans, UNC-6 provides positional information to the axons of developing neurons, probably by establishing a concentration gradient from the ventral to the dorsal side of the animal. Although the proper localization of UNC-6 is important for accurate neuronal network formation, little is known about how its localization is regulated. Here, to examine the localization mechanism for UNC-6, we generated C. elegans expressing UNC-6 tagged with the fluorescent protein Venus and identified 13 genes, which are involved in the cellular localization of VenusTUNC-6. For example, in unc-51, unc-14, and unc-104 mutants, the neurons showed an abnormal accumulation of VenusTUNC-6 in the cell body and less than normal level of VenusTUNC-6 in the axon. An aberrant accumulation of VenusTUNC-6 in muscle cells was seen in unc-18 and unc-68 mutants. unc-51, unc-14, and unc-104 mutants also showed defects in the guidance of dorso-ventral axons, suggesting that the abnormal localization of UNC-6 disturbed the positional information it provides. We propose that these genes regulate the process of UNC-6 secretion: expression, maturation, sorting, transport, or exocytosis. Our findings provide novel insight into the localization mechanism of the axon guidance molecule UNC-6/ Netrin.

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Section: Resultsmentioning

confidence: 99%

Genes Required for Cellular UNC-6/Netrin Localization in Caenorhabditis elegans

et al. 2010

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“…UNC-64 is a component of the core synaptic vesicle fusion machinery and is expressed throughout the nervous system (Ogawa et al 1998;Saifee et al 1998). In our transcriptome data, unc-64 transcripts were significantly upregulated in day 2 adult PG(2) UNC-119::GFP(+) gonads compared to day 2 adult control and day 2 adult PG(2) UNC-119::GFP(2) gonads.…”

Section: Unc-119::gfp(+) Gonads Turn On Numerous Genes Involved In Nementioning

confidence: 99%

Germ Granules Prevent Accumulation of Somatic Transcripts in the AdultCaenorhabditis elegansGermline

et al. 2017

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The germ cells of multicellular organisms protect their developmental potential through specialized mechanisms. A shared feature of germ cells from worms to humans is the presence of nonmembrane-bound, ribonucleoprotein organelles called germ granules. Depletion of germ granules in Caenorhabditis elegans (i.e., P granules) leads to sterility and, in some germlines, expression of the neuronal transgene unc-119::gfp and the muscle myosin MYO-3. Thus, P granules are hypothesized to maintain germ cell totipotency by preventing somatic development, although the mechanism by which P granules carry out this function is unknown. In this study, we performed transcriptome and single molecule RNA-FISH analyses of dissected P granule-depleted gonads at different developmental stages. Our results demonstrate that P granules are necessary for adult germ cells to downregulate spermatogenesis RNAs and to prevent the accumulation of numerous soma-specific RNAs. P granule-depleted gonads that express the unc-119::gfp transgene also express many other genes involved in neuronal development and concomitantly lose expression of germ cell fate markers. Finally, we show that removal of either of two critical P-granule components, PGL-1 or GLH-1, is sufficient to cause germ cells to express UNC-119::GFP and MYO-3 and to display RNA accumulation defects similar to those observed after depletion of P granules. Our data identify P granules as critical modulators of the germline transcriptome and guardians of germ cell fate.

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“…However, data from Drosophila melanogaster and squid indicate that syntaxin is not required for docking 31,42,43 . Furthermore, additional factors at the plasma membrane would be required, since UNC-18 and syntaxin are not restricted to active zones 8,44,45 . On the synaptic vesicle, potential targets include the Rab proteins, which are implicated in vesicle docking and exhibit genetic interactions with the Sec1-related proteins 46 .…”

Section: Models For Unc-18 Functionmentioning

confidence: 99%

Defects in synaptic vesicle docking in unc-18 mutants

et al. 2003

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Sec1-related proteins function in most, if not all, membrane trafficking pathways in eukaryotic cells. The Sec1-related protein required in neurons for synaptic vesicle exocytosis is UNC-18. Several models for UNC-18 function during vesicle exocytosis are under consideration. We have tested these models by characterizing unc-18 mutants of the nematode Caenorhabditis elegans. In the absence of UNC-18, the size of the readily releasable pool is severely reduced. Our results show that the near absence of fusion-competent vesicles is not caused by a reduction in syntaxin levels, by a mislocalization of syntaxin, by a defect in fusion or by a failure to open syntaxin during priming. Rather, we found a reduction of docked vesicles at the active zone in unc-18 mutants, suggesting that UNC-18 functions, directly or indirectly, as a facilitator of vesicle docking.Synaptic vesicles must be tethered to sites of release and then become competent for fusion with the plasma membrane. These processes are called docking and priming, respectively 1 . The molecular processes of docking are not well understood. Priming appears to involve the formation of trans-SNARE complexes, in which the synaptic vesicle protein synaptobrevin (also called VAMP) forms a helical bundle with the plasma membrane proteins syntaxin and . The formation of SNARE complexes is sufficient for membrane fusion in vitro 3 , but may require other components in vivo 4,5 .Another protein that is involved in synaptic vesicle exocytosis is . unc-18 mutants were first isolated in C. elegans on the basis of their severe locomotion defects 7 . The UNC-18 protein is similar to the yeast SEC1 protein 8 , and orthologs of UNC-18 function at the synapses of fruit flies (Rop) 9 and vertebrates (Muncl8-1; also known as Stxbpl, N-secl, Rb-secl) 10 . Genetic studies of UNC-18 in various organisms suggest that UNC-18 is required for synaptic vesicle exocytosis. For example, unc-18 mutants in C. elegans are severely paralyzed and are resistant to inhibitors of cholinesterase but sensitive to acetylcholine (ACh) receptor agonists 11 , implicating UNC-18 in the exocytosis of ACh.

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Functional Properties of the unc-64 Gene Encoding aCaenorhabditis elegans Syntaxin

Abstract: Phenotypes of Caenorhabditis elegans unc-18 and unc-64 gene mutations are similar. While unc-18 is known to be essential for normal synaptic transmission (Hosono, R., Hekimi, S., Kamiya, Y., Sassa, T., Murakami, S., Nishiwaki, S., Miwa, J., Taketo

Cited by 76 publications

References 25 publications

Genes Required for Cellular UNC-6/Netrin Localization in Caenorhabditis elegans

Genes Required for Cellular UNC-6/Netrin Localization in Caenorhabditis elegans

Germ Granules Prevent Accumulation of Somatic Transcripts in the AdultCaenorhabditis elegansGermline

Defects in synaptic vesicle docking in unc-18 mutants

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