Evidence map›Paper›PMID 41759732›Full record

ArticleThe Journal of biological chemistry2026

The AAA-ATPase Yta4 inhibits the interaction between Ppa2 and Atg43 to promote Atg43 phosphorylation and mitophagy.

Ke Liu, Jiajia He, Yifan Wu, Chenhui Zhao, Shuaijie Yan, Fangyuan Xiong, Xing Liu, Xuebiao Yao, Chuanhai Fu

Abstract read
In one paragraph

Article in The Journal of biological chemistry, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
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1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

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Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

9 authors.

Ke LiuMOE Key Laboratory for Cellular Dynamics & School of Life Sciences, Division of Life Sciences and Medicine, University of Science and Technology of China, Hefei, China; Anhui Key Laboratory for Chemical Biology and New Quality Medicine & Hefei National Research Center for Interdisciplinary Sciences at the Microscale, School of Life Sciences, University of Science and Technology of China, Hefei, China.
Jiajia HeMOE Key Laboratory for Cellular Dynamics & School of Life Sciences, Division of Life Sciences and Medicine, University of Science and Technology of China, Hefei, China; Anhui Key Laboratory for Chemical Biology and New Quality Medicine & Hefei National Research Center for Interdisciplinary Sciences at the Microscale, School of Life Sciences, University of Science and Technology of China, Hefei, China.
Yifan WuMOE Key Laboratory for Cellular Dynamics & School of Life Sciences, Division of Life Sciences and Medicine, University of Science and Technology of China, Hefei, China; Anhui Key Laboratory for Chemical Biology and New Quality Medicine & Hefei National Research Center for Interdisciplinary Sciences at the Microscale, School of Life Sciences, University of Science and Technology of China, Hefei, China.
Chenhui ZhaoMOE Key Laboratory for Cellular Dynamics & School of Life Sciences, Division of Life Sciences and Medicine, University of Science and Technology of China, Hefei, China; Anhui Key Laboratory for Chemical Biology and New Quality Medicine & Hefei National Research Center for Interdisciplinary Sciences at the Microscale, School of Life Sciences, University of Science and Technology of China, Hefei, China.
Shuaijie YanMOE Key Laboratory for Cellular Dynamics & School of Life Sciences, Division of Life Sciences and Medicine, University of Science and Technology of China, Hefei, China; Anhui Key Laboratory for Chemical Biology and New Quality Medicine & Hefei National Research Center for Interdisciplinary Sciences at the Microscale, School of Life Sciences, University of Science and Technology of China, Hefei, China.
Fangyuan XiongMOE Key Laboratory for Cellular Dynamics & School of Life Sciences, Division of Life Sciences and Medicine, University of Science and Technology of China, Hefei, China; Anhui Key Laboratory for Chemical Biology and New Quality Medicine & Hefei National Research Center for Interdisciplinary Sciences at the Microscale, School of Life Sciences, University of Science and Technology of China, Hefei, China.
Xing LiuMOE Key Laboratory for Cellular Dynamics & School of Life Sciences, Division of Life Sciences and Medicine, University of Science and Technology of China, Hefei, China; Anhui Key Laboratory for Chemical Biology and New Quality Medicine & Hefei National Research Center for Interdisciplinary Sciences at the Microscale, School of Life Sciences, University of Science and Technology of China, Hefei, China.
Xuebiao YaoMOE Key Laboratory for Cellular Dynamics & School of Life Sciences, Division of Life Sciences and Medicine, University of Science and Technology of China, Hefei, China; Anhui Key Laboratory for Chemical Biology and New Quality Medicine & Hefei National Research Center for Interdisciplinary Sciences at the Microscale, School of Life Sciences, University of Science and Technology of China, Hefei, China.
Chuanhai FuMOE Key Laboratory for Cellular Dynamics & School of Life Sciences, Division of Life Sciences and Medicine, University of Science and Technology of China, Hefei, China; Anhui Key Laboratory for Chemical Biology and New Quality Medicine & Hefei National Research Center for Interdisciplinary Sciences at the Microscale, School of Life Sciences, University of Science and Technology of China, Hefei, China. Electronic address: chuanhai@ustc.edu.cn.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

AAA-ATPase Yta4/Msp1/ATAD1 is a well-known quality control factor that clears mistargeted tail-anchored proteins and precursor proteins on mitochondria. However, whether Yta4 preserves mitochondrial homeostasis through alternate pathways remains unclear. Traditionally, mitophagy has been recognized as a crucial pathway for eliminating dysfunctional mitochondria, thereby ensuring the maintenance of mitochondrial homeostasis. In this study, we unveil a novel role for Yta4 in sustaining mitochondrial homeostasis by facilitating mitophagy in fission yeast. The absence of Yta4 delays the phosphorylation of the mitophagy receptor Atg43 and specifically inhibits mitophagy. Additionally, Atg43 phosphorylation sites Ser32, Ser35, and Ser36, which are crucial for mitophagy, were identified. We further found that the phosphatase Ppa2 plays a major role in Atg43 dephosphorylation and inhibits excessive mitophagy. Yta4 physically interacts with both Atg43 and Ppa2, and coordinates with Ppa2 to modulate Atg43 phosphorylation and mitophagy. Moreover, Yta4 and Ppa2 bind to the same cytosolic region of Atg43, and Yta4 inhibits the interaction between Atg43 and Ppa2. Collectively, our findings suggest that Yta4 promotes mitophagy by ensuring the effectiveness of Atg43 phosphorylation. Thus, our findings reveal the novel function of Yta4 in regulating mitophagy and expand the understanding of the molecular mechanisms underlying mitophagy in fission yeast.

Indexed as

Adenosine TriphosphatasesAutophagy-Related ProteinsMitophagySchizosaccharomycesSchizosaccharomyces pombe ProteinsMitochondriaPhosphorylationAdenosine TriphosphatasesAutophagy-Related ProteinsSchizosaccharomyces pombe ProteinsATAD1fission yeastmitochondriaphosphatasephosphorylationPP2A

Identifiers

PMID41759732
PMCPMC13018932

What OpenQuestion holds

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LicenceCC BY-NC-ND
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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.