Redox regulation of memory formation by Rrp1 in <i>Drosophila</i>

C Cheng-Tzu Hsu (Institute of Biotechnology and Department of Life Science, National Tsing-Hua University) C Chun-Chao Chen (Institute of Precision Medicine, College of Medicine, National Sun Yat-sen University) Y Yu-Ling Hung (Institute of Biotechnology and Department of Life Science, National Tsing-Hua University) Y Ya-Ting Yang (Institute of Biotechnology and Department of Life Science, National Tsing-Hua University) Y Yen-Hua Chiu (Institute of Biotechnology and Department of Life Science, National Tsing-Hua University) S Sing-Shien Fong (Institute of Biotechnology and Department of Life Science, National Tsing-Hua University) J Jung-Hsuan Yang (Institute of Biotechnology and Department of Life Science, National Tsing-Hua University) Z Zheng-Wen Wu (Institute of Biotechnology and Department of Life Science, National Tsing-Hua University) J Jian-Wei Liou (Institute of Biotechnology and Department of Life Science, National Tsing-Hua University) H Hsuan-Wen Lin (Department of Biomedical Science and Technology, College of Medicine, National Sun Yat-sen University) K Kuan-Lin Feng (Brain Research Center, National Tsing Hua University) J Jia-Ling Yang (Institute of Biotechnology and Department of Life Science, National Tsing-Hua University) A Ann-Shyn Chiang (Institute of Biotechnology and Department of Life Science, National Tsing-Hua University)

Abstract

Long-term memory (LTM) formation requires precise gene regulation, yet the role of redox activity in this process remains poorly understood. Here, we identify Drosophila recombination repair protein 1 (Rrp1), a homolog of human apurinic/apyrimidinic endonuclease 1 (APE1), as a key redox regulator of LTM. In paired dorsal-anterior-lateral neurons—critical for aversive olfactory memory—Rrp1 knockdown impairs memory formation, whereas its overexpression enhances retention. Pharmacological inhibition of Rrp1 redox activity with E3330 suppresses Period and CaMKII expression, disrupting LTM formation. Notably, human APE1 redox activity rescues memory deficits in Rrp1-deficient flies, promotes de novo Period synthesis, and facilitates LTM formation. Moreover, Rrp1 is required for CREBA-mediated LTM acceleration, revealing a redox-dependent link between transcriptional regulation and memory persistence. These findings establish Rrp1 as a critical modulator of LTM in Drosophila and highlight redox regulation as a conserved mechanism underlying memory formation.

Article Details

Volume / Issue Vol. 122, Issue 48
Published December 02, 2025
ISSN 0027-8424
Publisher National Academy of Sciences

Authors (13)

C

Cheng-Tzu Hsu

Institute of Biotechnology and Department of Life Science, National Tsing-Hua University

C

Chun-Chao Chen

Institute of Precision Medicine, College of Medicine, National Sun Yat-sen University

Y

Yu-Ling Hung

Institute of Biotechnology and Department of Life Science, National Tsing-Hua University

Y

Ya-Ting Yang

Institute of Biotechnology and Department of Life Science, National Tsing-Hua University

Y

Yen-Hua Chiu

Institute of Biotechnology and Department of Life Science, National Tsing-Hua University

S

Sing-Shien Fong

Institute of Biotechnology and Department of Life Science, National Tsing-Hua University

J

Jung-Hsuan Yang

Institute of Biotechnology and Department of Life Science, National Tsing-Hua University

Z

Zheng-Wen Wu

Institute of Biotechnology and Department of Life Science, National Tsing-Hua University

J

Jian-Wei Liou

Institute of Biotechnology and Department of Life Science, National Tsing-Hua University

H

Hsuan-Wen Lin

Department of Biomedical Science and Technology, College of Medicine, National Sun Yat-sen University

K

Kuan-Lin Feng

Brain Research Center, National Tsing Hua University

J

Jia-Ling Yang

Institute of Biotechnology and Department of Life Science, National Tsing-Hua University

A

Ann-Shyn Chiang

Institute of Biotechnology and Department of Life Science, National Tsing-Hua University