Evidence map›Paper›PMID 37232206›Full record

ArticleJournal of cell science2023

Optogenetically engineered Ca2+ oscillation-mediated DRP1 activation promotes mitochondrial fission and cell death.

Yi-Shyun Lai, Cheng-Chi Chang, Yong-Yi Chen, Thi My Hang Nguyen, Jixuan Xu, Ying-Chi Chen, Yu-Fen Chang, Chia-Yih Wang, Pai-Sheng Chen, Shih-Chieh Lin and 3 more

Open access · hybridAbstract read
In one paragraph

Article in Journal of cell science, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
1.4field-weighted citation impact, top 19% of its field
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

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

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

10 citing papers in PubMed, 9 citations in OpenAlex.

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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

13 authors at 1 institution in 1 country.

Yi-Shyun LaiDepartment of Biomedical Engineering, National Cheng Kung University, Tainan 701, Taiwan.ORCID 0000-0002-9538-6705
Cheng-Chi ChangDepartment of Biomedical Engineering, National Cheng Kung University, Tainan 701, Taiwan.ORCID 0000-0003-4798-4927
Yong-Yi ChenDepartment of Biomedical Engineering, National Cheng Kung University, Tainan 701, Taiwan.ORCID 0000-0003-0637-3740
Thi My Hang NguyenDepartment of Biomedical Engineering, National Cheng Kung University, Tainan 701, Taiwan.ORCID 0000-0002-5330-816X
Jixuan XuDepartment of Biomedical Engineering, National Cheng Kung University, Tainan 701, Taiwan.ORCID 0000-0002-2015-8636
Ying-Chi ChenDepartment of Chemistry, National Cheng Kung University, Tainan 701, Taiwan.ORCID 0000-0003-3711-0329
Yu-Fen ChangLumiSTAR Biotechnology, Taipei 115, Taiwan.ORCID 0000-0002-9092-7306
Chia-Yih WangDepartment of Cell Biology and Anatomy, National Cheng Kung University, Tainan 701, Taiwan.ORCID 0000-0002-9196-0802
Pai-Sheng ChenDepartment of Medical Laboratory Science and Biotechnology, National Cheng Kung University, Tainan 701, Taiwan.ORCID 0000-0003-0513-1467
Shih-Chieh LinInstitute of Basic Medical Sciences, National Cheng Kung University, Tainan 701, Taiwan.ORCID 0000-0002-9967-5037
I-Chen PengDepartment of Life Sciences, National Cheng Kung University, Tainan 701, Taiwan.ORCID 0000-0001-5826-500X
Shaw-Jenq TsaiInstitute of Basic Medical Sciences, National Cheng Kung University, Tainan 701, Taiwan.ORCID 0000-0002-3569-5813
Wen-Tai ChiuDepartment of Biomedical Engineering, National Cheng Kung University, Tainan 701, Taiwan.ORCID 0000-0003-0310-0675
National Cheng Kung University · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Mitochondrial dynamics regulate the quality and morphology of mitochondria. Calcium (Ca2+) plays an important role in regulating mitochondrial function. Here, we investigated the effects of optogenetically engineered Ca2+ signaling on mitochondrial dynamics. More specifically, customized illumination conditions could trigger unique Ca2+ oscillation waves to trigger specific signaling pathways. In this study, we found that modulating Ca2+ oscillations by increasing the light frequency, intensity and exposure time could drive mitochondria toward the fission state, mitochondrial dysfunction, autophagy and cell death. Moreover, illumination triggered phosphorylation at the Ser616 residue but not the Ser637 residue of the mitochondrial fission protein, dynamin-related protein 1 (DRP1, encoded by DNM1L), via the activation of Ca2+-dependent kinases CaMKII, ERK and CDK1. However, optogenetically engineered Ca2+ signaling did not activate calcineurin phosphatase to dephosphorylate DRP1 at Ser637. In addition, light illumination had no effect on the expression levels of the mitochondrial fusion proteins mitofusin 1 (MFN1) and 2 (MFN2). Overall, this study provides an effective and innovative approach to altering Ca2+ signaling for controlling mitochondrial fission with a more precise resolution than pharmacological approaches in the temporal dimension.

Indexed as

CalciumMitochondrial DynamicsCell DeathDynaminsMitochondriaMitochondrial ProteinsPhosphorylationCalciumDynaminsMitochondrial ProteinsCa2+ oscillationDRP1Mitochondrial fissionOptogenetics

Identifiers

PMID37232206
PMCPMC10323238
OpenAlexW4378347507

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.