Skip to main content
MIT Mobile homeEvents - old home
Event Detail

SCSB Lunch Series: Role of FMRP interactions with presynaptic ion channels in Fragile X Syndrome

Fri May 10, 2024 12:00–1:00 PM

Location

Simons Center Conference room, 46-6011, 46-6011

Description

Date: Friday, May 10, 2024 Time: 12:00pm – 1:00pm Location: Simons Center Conference room 46-6011 + Zoom Meeting: https://mit.zoom.us/j/91647033337Speaker: Chhavi Sood, Ph.D. Affiliation: Simons Postdoctoral Fellow, Littleton Lab, Picower Institute, BCS, Department of Biology, MITTalk title: Role of FMRP interactions with presynaptic ion channels in Fragile X SyndromeAbstract: Synaptic vesicle (SV) fusion occurs in response to Ca2+ influx from voltage-gated Ca2+ channels (VGCCs) at AZs. Multiple conserved proteins cluster SVs and VGCCs at the AZs. Additionally, BK channels (Ca2+-activated K+ channels) also cluster at AZs to rapidly repolarize the presynaptic membrane, close VGCCs, and terminate Ca2+ influx and SV release. Using the Drosophila model of Fragile X Syndrome (FXS) and neuromuscular junction, I aim to determine how FMRP controls VGCC and BK channel synaptic delivery and AZ abundance and how dysregulation of these interactions contributes to synaptic defects in FXS.
  • SCSB Lunch Series: Role of FMRP interactions with presynaptic ion channels in Fragile X Syndrome
    Date: Friday, May 10, 2024 Time: 12:00pm – 1:00pm Location: Simons Center Conference room 46-6011 + Zoom Meeting: https://mit.zoom.us/j/91647033337Speaker: Chhavi Sood, Ph.D. Affiliation: Simons Postdoctoral Fellow, Littleton Lab, Picower Institute, BCS, Department of Biology, MITTalk title: Role of FMRP interactions with presynaptic ion channels in Fragile X SyndromeAbstract: Synaptic vesicle (SV) fusion occurs in response to Ca2+ influx from voltage-gated Ca2+ channels (VGCCs) at AZs. Multiple conserved proteins cluster SVs and VGCCs at the AZs. Additionally, BK channels (Ca2+-activated K+ channels) also cluster at AZs to rapidly repolarize the presynaptic membrane, close VGCCs, and terminate Ca2+ influx and SV release. Using the Drosophila model of Fragile X Syndrome (FXS) and neuromuscular junction, I aim to determine how FMRP controls VGCC and BK channel synaptic delivery and AZ abundance and how dysregulation of these interactions contributes to synaptic defects in FXS.