Synaptotagmin-mediated plasma membrane homeostasis is required to recruit the endocytic machinery during cold stress
- 1Universidad de Malaga - IHSM La Mayora UMA-CSIC
Abstract
Endocytosis depends on plasma membrane (PM) lipid composition, yet how plants sustain endocytic machinery recruitment during stress remains unclear. We investigated whether synaptotagmins SYT1 and SYT3 function in membrane homeostasis and endocytosis in Arabidopsis thaliana. In this work, we revealed that cold stress reversibly blocked FM4-64 internalization in syt1syt3 double mutants by displacing peripheral and core TPC subunits from the PM. Loss of SYT1 reduced brassinosteroid receptor internalization during cold stress, while double mutants showed enhanced brassinosteroid signaling. SYTs and VAP27 genes showed a condition-dependent genetic interaction in endocytosis: the syt1/vap27-1/vap27-3 triple mutant resembles vap27-1/vap27-3 under control conditions and syt1 during cold stress, suggesting overlapping contributions to endocytic regulation. Using molecular dynamics simulations of protein-membrane interactions, phosphoinositide depletion combined with increased diacylglycerol weakened TPC core membrane association. Our findings identify SYT1 and SYT3 as essential components for sustaining endocytosis during abiotic stress and support a model in which lipid homeostasis at endoplasmic reticulum-PM contact sites preserves the membrane composition required for TPC-dependent endocytosis.
Related
- PfATG18 links V-ATPase assembly to endocytic membrane dynamics in malaria parasites
- Stress-induced Membrane Insertion at the β-Barrel Assembly Machinery Complex Regulates BepA Metalloprotease Activity
- Stress-induced membrane insertion at the β-barrel assembly machinery complex regulates BepA metalloprotease activity
- The Membrane Stress Response Buffers Lethal Effects of Lipid Disequilibrium by Reprogramming the Protein Homeostasis Network
- Mechanistic Insights into MYO1C-Mediated Rhodopsin Trafficking and Rod Photoreceptor Homeostasis.
BibTeX
@misc{aznarmoreno2026synaptotagminmediated,
title = {{Synaptotagmin-mediated plasma membrane homeostasis is required to recruit the endocytic machinery during cold stress}},
author = {J. A. Aznar-Moreno and A. Del Espino and J. Moya-Cuevas and J. Perez-Sancho and G. Wilbrink and M. Neubergerova and A. De Meyer and S. Vanneste and P. Grones and L. Rubio and R. Pleskot and D. Van Damme and V. Amorim-Silva and M. A. Botella},
howpublished = {bioRxiv},
year = {2026},
month = oct,
doi = {10.64898/2026.10.17.759674},
url = {https://www.biorxiv.org/content/10.64898/2026.10.17.759674v1},
note = {CC BY-NC-ND},
}
RIS
TY - UNPB
TI - Synaptotagmin-mediated plasma membrane homeostasis is required to recruit the endocytic machinery during cold stress
AU - J. A. Aznar-Moreno
AU - A. Del Espino
AU - J. Moya-Cuevas
AU - J. Perez-Sancho
AU - G. Wilbrink
AU - M. Neubergerova
AU - A. De Meyer
AU - S. Vanneste
AU - P. Grones
AU - L. Rubio
AU - R. Pleskot
AU - D. Van Damme
AU - V. Amorim-Silva
AU - M. A. Botella
PY - 2026
DA - 2026/10/17
PB - bioRxiv
DO - 10.64898/2026.10.17.759674
UR - https://www.biorxiv.org/content/10.64898/2026.10.17.759674v1
AB - Endocytosis depends on plasma membrane (PM) lipid composition, yet how plants sustain endocytic machinery recruitment during stress remains unclear. We investigated whether synaptotagmins SYT1 and SYT3 function in membrane homeostasis and endocytosis in Arabidopsis thaliana. In this work, we revealed that cold stress reversibly blocked FM4-64 internalization in syt1syt3 double mutants by displacing peripheral and core TPC subunits from the PM. Loss of SYT1 reduced brassinosteroid receptor internalization during cold stress, while double mutants showed enhanced brassinosteroid signaling. SYTs and VAP27 genes showed a condition-dependent genetic interaction in endocytosis: the syt1/vap27-1/vap27-3 triple mutant resembles vap27-1/vap27-3 under control conditions and syt1 during cold stress, suggesting overlapping contributions to endocytic regulation. Using molecular dynamics simulations of protein-membrane interactions, phosphoinositide depletion combined with increased diacylglycerol weakened TPC core membrane association. Our findings identify SYT1 and SYT3 as essential components for sustaining endocytosis during abiotic stress and support a model in which lipid homeostasis at endoplasmic reticulum-PM contact sites preserves the membrane composition required for TPC-dependent endocytosis.
ER -