203 results for “unc-31”
Genes (1)
UNCoordinated 31
Papers (48)
Immunomodulation plays a pivotal role in maintaining immune homeostasis, defending against pathogens, and regulating various biological processes. Tetraspanins (TSPs), a highly conserved transmembrane protein superfamily, are predominantly expressed ...
GABAergic neurotransmission constitutes a major inhibitory signaling mechanism that plays crucial roles in central nervous system physiology and immune cell immunomodulation. However, its roles in innate immunity remain unclear. Here, we report that ...
An animal's behavioral and physiological response to stressors includes changes to its responses to stimuli. How such changes occur is not well understood. Here we describe a Caenorhabditis elegans quiescent behavior, post-response quiescence (PRQ), ...
In its native environment of rotting vegetation, the soil nematode Caenorhabditis elegans encounters a range of bacteria. This includes species from the ESKAPE group of pathogens that pose a clinical problem in acquired hospital infections. Here, we ...
Assembly of SNARE complexes that mediate neurotransmitter release requires opening of a 'closed' conformation of UNC-64/syntaxin. Rescue of unc-13/Munc13 mutant phenotypes by overexpressed open UNC-64/syntaxin suggested a specific function of UNC-13/...
Cyclic AMP (cAMP) signaling augments synaptic transmission, but because many targets of cAMP and protein kinase A (PKA) may be involved, mechanisms underlying this pathway remain unclear. To probe this mechanism, we used optogenetic stimulation of cA...
Amyotrophic lateral sclerosis (ALS) is a neurodegenerative disease thought to employ cell non-autonomous mechanisms where neuronal injury engages immune responses to influence disease progression. Here we show that the expression of mutant proteins c...
How an animal matches feeding to food availability is a key question for energy homeostasis. We addressed this in the nematode Caenorhabditis elegans, which couples feeding to the presence of its food (bacteria) by regulating pharyngeal activity (pum...
Precise and accurate axon tract formation is an essential aspect of brain development. This is achieved by the migration of early outgrowing axons (pioneers) allowing later outgrowing axons (followers) to extend toward their targets in the embryo. In...
Pore-forming toxins (PFTs) are abundant bacterial virulence factors that attack host cell plasma membranes. Host defense mechanisms against PFTs described to date all function in the host tissue that is directly attacked by the PFT. Here we character...
Claims (154)
By performing calcium imaging on the ADF neurons in synaptic signaling ( unc-13 ) and peptidergic ( unc-31 ) signaling mutant backgrounds, we show that the ADF neurons require input from other neurons, likely the ASK neurons, to respond to food extracts.
Loss of UNC-31 causes multiple phenotypes in C. elegans including reduced motility, retention of late-stage eggs, and reduction in evoked synaptic release.
Consequently, the function of endogenous daf-28, but not that of ins-6 and ins-4, is independent of unc-31.
By performing calcium imaging on the ADF neurons in synaptic signaling (unc-13) and peptidergic (unc-31) signaling mutant backgrounds, we show that the ADF neurons require input from other neurons to respond to food extracts.
Notably, we found that CPX-1's clamping function is dependent on UNC-31 and is sensitive to external Ca2+.
Here, using C. elegans as the model animal system, we find that the head sensory neurons show aberrant positional layout in neurotransmitter (unc-13), but not in neuropeptide (unc-31), release mutants.
This process requires the dense-core vesicle regulator UNC-31/CAPS, as unc-31 null mutations eliminate both the increased mPSC amplitude and elevated ACR-16 expression in cpx-1 mutants.
Consequently, the function of endogenous daf-28, but not that of ins-6 and ins-4, is independent of unc-31.
Consequently, the function of endogenous daf-28, but not that of ins-6 and ins-4, is independent of unc-31.
Using the auxin-inducible degradation system, we depleted UNC-31 postembryonically from the hermaphrodite nervous system and revealed defects in egg laying, locomotion, and vesicle release that were comparable to those in unc-31 null mutant animals.