PhD Scientific Days 2026

Budapest, 16-18 June 2026

Molecular Medicine 3.

The role of SERCA Ca²⁺ transporter in Autophagy

Előadó neve

Ms. Kenzhebayeva, Zhanerke

Neptune code

E616XY

Előadó munkahelye

Etvos Lorand University

Előadó telefonszáma

06205399515

Előadó e-mail címe

sstifour@gmail.com

Az előadás címe

The role of SERCA Ca²⁺ transporter in Autophagy

Szerző(k) neve és munkahelye

Zhanerke Kenzhebayeva1,2, Sarolta Tóth2, Ágnes Enyedi2, Szabolcs Takáts1

1: Department of Anatomy, Cell and Developmental Biology, Eotvos Lorand University, Budapest
2: Department of Transfusiology, Semmelweis University, Budapest

Bemutatás módja

Szóbeli

Szekció

Molecular Medicine 3.

Language of the presentation

English

Preferred session

Molecular Medicine

Összefoglaló szövege

Introduction
The Sarco/endoplasmic reticulum Ca²⁺ ATPase (SERCA) pumps Ca²⁺ into the ER, maintaining Ca²⁺ homeostasis and supporting downstream cellular processes, including autophagy. Autophagy is a lysosomal degradation pathway critical for cellular homeostasis under stress, proceeding through phagophore formation, autophagosome biogenesis, and autolysosomal cargo degradation. Although Ca²⁺ signaling and SERCA have been implicated in autophagy regulation, the precise molecular mechanisms remain poorly understood.
Aims
To investigate the role of SERCA and its interacting partners in the regulation of autophagy, with particular focus on early autophagic membrane dynamics in a Drosophila adipose tissue model.
Methods
SERCA and VMP1 (Vacuolar Membrane Protein 1) were silenced in Drosophila fat body using RNAi. Autophagic flux was assessed by monitoring the cargo receptor p62. Fluorescent immunolabeling and electron microscopy (EM) were used to characterize mitochondrial integrity, phagophore morphology, and VMP1 subcellular localization. Vps13D knockdown was additionally performed to probe functional interactions.
Results
Silencing of SERCA or VMP1 caused accumulation of p62, damaged mitochondria, and stalled phagophores unable to mature into autophagosomes. VMP1 subcellular localization was found to be SERCA-dependent. Knockdown of Vps13D, a known VMP1 interactor involved in mitophagy, phenocopied these defects, also resulting in downregulated autophagy and phagophore arrest.
Conclusion
SERCA plays a critical role in the early steps of autophagy, specifically in phagophore formation, likely through regulating VMP1 localization and its functional cooperation with Vps13D.
Funding:
Excellence Fund of ELTE (EKA_2022/045-P302-1)
NKFIH (OTKA FK_142508)
Hungarian Academy of Sciences (BO/00400/23)

University

Semmelweis University

Other university, not listed above

Etvos Lorand University

Supervisor

Ágnes Enyedi, Szabolcs Takáts

Publication of my abstract

I give consent to the publication of my abstract on the website of the congress.

phd.section.field

in doctoral studies after complex exam (PhD)

Kind

Szabad

Status

elfogadva

Accepted presentation method

szóbeli

Előadás fájl jóváhagyás

nem rendelkezett róla

Előadó

9824

Start

10:15

End

10:25