Evidence map›Paper›PMID 22621211›Full record

ArticleJournal of biomedical science2012

Autophagy-related gene 7 is downstream of heat shock protein 27 in the regulation of eye morphology, polyglutamine toxicity, and lifespan in Drosophila.

Shih-Fen Chen, Ming-Lun Kang, Yi-Chun Chen, Hong-Wen Tang, Cheng-Wen Huang, Wan-Hua Li, Chun-Pu Lin, Chao-Yung Wang, Pei-Yu Wang, Guang-Chao Chen and 1 more

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In one paragraph

Article in Journal of biomedical science, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
2.1field-weighted citation impact, top 13% 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

30 citing papers in PubMed, 48 citations in OpenAlex.

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  8. The Importance of mTORC1-Autophagy Axis for Skeletal Muscle Diseases.International journal of molecular sciences · 2022
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  18. On the Fly: Recent Progress on Autophagy and Aging in Drosophila.Frontiers in cell and developmental biology · 2019
    Review
  19. Article
  20. Article
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

11 authors at 4 institutions in 1 country.

Shih-Fen ChenInstitute of Biotechnology, National Tsing Hua University, 101, Section 2, Kuang-Fu Road, HsinChu, 30013, Taiwan.
Ming-Lun Kang
Yi-Chun Chen
Hong-Wen Tang
Cheng-Wen Huang
Wan-Hua Li
Chun-Pu Lin
Chao-Yung Wang
Pei-Yu Wang
Guang-Chao Chen
Horng-Dar Wang
National Tsing Hua University · TWInstitute of Biological Chemistry, Academia Sinica · TWChang Gung University · TWNational Chengchi University · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundAutophagy and molecular chaperones both regulate protein homeostasis and maintain important physiological functions. Atg7 (autophagy-related gene 7) and Hsp27 (heat shock protein 27) are involved in the regulation of neurodegeneration and aging. However, the genetic connection between Atg7 and Hsp27 is not known.

methodsThe appearances of the fly eyes from the different genetic interactions with or without polyglutamine toxicity were examined by light microscopy and scanning electronic microscopy. Immunofluorescence was used to check the effect of Atg7 and Hsp27 knockdown on the formation of autophagosomes. The lifespan of altered expression of Hsp27 or Atg7 and that of the combination of the two different gene expression were measured.

resultsWe used the Drosophila eye as a model system to examine the epistatic relationship between Hsp27 and Atg7. We found that both genes are involved in normal eye development, and that overexpression of Atg7 could eliminate the need for Hsp27 but Hsp27 could not rescue Atg7 deficient phenotypes. Using a polyglutamine toxicity assay (41Q) to model neurodegeneration, we showed that both Atg7 and Hsp27 can suppress weak, toxic effect by 41Q, and that overexpression of Atg7 improves the worsened mosaic eyes by the knockdown of Hsp27 under 41Q. We also showed that overexpression of Atg7 extends lifespan and the knockdown of Atg7 or Hsp27 by RNAi reduces lifespan. RNAi-knockdown of Atg7 expression can block the extended lifespan phenotype by Hsp27 overexpression, and overexpression of Atg7 can extend lifespan even under Hsp27 knockdown by RNAi.

conclusionsWe propose that Atg7 acts downstream of Hsp27 in the regulation of eye morphology, polyglutamine toxicity, and lifespan in Drosophila.

Indexed as

DrosophilaEyeAnimalsAutophagyAutophagy-Related Protein 7Drosophila ProteinsEpistasis, GeneticGene Expression Regulation, DevelopmentalHSP27 Heat-Shock ProteinsPeptidesRNA InterferenceAtg7 protein, DrosophilaAutophagy-Related Protein 7Drosophila ProteinsHSP27 Heat-Shock ProteinsPeptidespolyglutamine

Identifiers

PMID22621211
PMCPMC3483682
OpenAlexW2119222471

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

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.