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Peer-reviewedCC BYMicroPublication biology

Loss of periactive-zone scaffold proteins does not enhance neurotransmission defects in cla-1(ΔL) mutants.

  • Elaina Cote1
  • Zhao Xuan1
  1. 1School of Biology and Ecology, University of Maine, Orono, ME, United States.
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Abstract

Efficient synaptic transmission requires coordinated exocytosis and endocytosis at the active zone and adjacent periactive zone, but whether scaffold proteins from these two presynaptic compartments function cooperatively remains unclear. Because the active-zone scaffold CLA-1 L genetically interacts with the periactive-zone scaffolds EHS-1 and ITSN-1 during presynaptic ATG-9 sorting, we tested whether these interactions extend to neurotransmission using aldicarb assays. Although cla-1 (ΔL) , ehs-1 (null) , and itsn-1 (null) mutants each exhibited mild aldicarb resistance, neither ehs-1 (null) nor itsn-1 (null) enhanced the neurotransmission defect of cla-1 (ΔL) mutants.

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Cite

BibTeXRIS
BibTeX
@article{cote2026loss,
  title = {{Loss of periactive-zone scaffold proteins does not enhance neurotransmission defects in cla-1(ΔL) mutants.}},
  author = {Elaina Cote and Zhao Xuan},
  journal = {MicroPublication biology},
  year = {2026},
  month = oct,
  doi = {10.17912/micropub.biology.002331},
  url = {https://europepmc.org/article/MED/42903352},
  note = {CC BY},
}
RIS
TY  - JOUR
TI  - Loss of periactive-zone scaffold proteins does not enhance neurotransmission defects in cla-1(ΔL) mutants.
AU  - Elaina Cote
AU  - Zhao Xuan
PY  - 2026
DA  - 2026/10/05
JO  - MicroPublication biology
DO  - 10.17912/micropub.biology.002331
UR  - https://europepmc.org/article/MED/42903352
AB  - Efficient synaptic transmission requires coordinated exocytosis and endocytosis at the active zone and adjacent periactive zone, but whether scaffold proteins from these two presynaptic compartments function cooperatively remains unclear. Because the active-zone scaffold CLA-1 L genetically interacts with the periactive-zone scaffolds EHS-1 and ITSN-1 during presynaptic ATG-9 sorting, we tested whether these interactions extend to neurotransmission using aldicarb assays. Although cla-1 (ΔL) , ehs-1 (null) , and itsn-1 (null) mutants each exhibited mild aldicarb resistance, neither ehs-1 (null) nor itsn-1 (null) enhanced the neurotransmission defect of cla-1 (ΔL) mutants.
SN  - 2578-9430
ER  -