Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Pivot Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Target Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Query: EC:3.1.1.7 (
acetylcholinesterase
)
28,390
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
Precise signaling at the neuromuscular junction (NMJ) is essential for proper muscle contraction. In the
Caenorhabditis elegans
pharynx, acetylcholine (ACh) released from the MC and M4 motor neurons stimulates two different types of contractions in adjacent muscle cells, termed pumping and isthmus peristalsis. MC stimulates rapid pumping through the nicotinic ACh receptor
EAT-2
, which is tightly localized at the MC NMJ, and
eat-2
mutants exhibit a slow pump rate. Surprisingly, we found that
eat-2
mutants also hyperstimulated peristaltic contractions, and that they were characterized by increased and prolonged Ca
2+
transients in the isthmus muscles. This hyperstimulation depends on cross talk with the GAR-3 muscarinic ACh receptor as
gar-3
mutation specifically suppressed the prolonged contraction and increased Ca
2+
observed in
eat-2
mutant peristalses. Similar GAR-3-dependent hyperstimulation was also observed in mutants lacking the
ace-3
acetylcholinesterase
, and we suggest that NMJ defects in
eat-2
and
ace-3
mutants result in ACh stimulation of extrasynaptic GAR-3 receptors in isthmus muscles.
gar-3
mutation also suppressed slow larval growth and prolonged life span phenotypes that result from dietary restriction in
eat-2
mutants, indicating that cross talk with the GAR-3 receptor has a long-term impact on feeding behavior and
eat-2
mutant phenotypes.
...
PMID:Cross Talk with the GAR-3 Receptor Contributes to Feeding Defects in
Caenorhabditis elegans eat-2
Mutants. 3089 71
