Evidence map›Paper›PMID 33561224›Full record

ArticleG3 (Bethesda, Md.)2021

Heat shock proteins and small nucleolar RNAs are dysregulated in a Drosophila model for feline hypertrophic cardiomyopathy.

Christian A Tallo, Laura H Duncan, Akihiko H Yamamoto, Joshua D Slaydon, Gunjan H Arya, Lavanya Turlapati, Trudy F C Mackay, Mary A Carbone

Open access · goldAbstract read
In one paragraph

Article in G3 (Bethesda, Md.), 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
0.6field-weighted citation impact, top 27% 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

9 citing papers in PubMed, 10 citations in OpenAlex.

  1. Review
  2. Review
  3. Review
  4. Review
  5. Genetic Basis of Hypertrophic Cardiomyopathy in Cats.Current issues in molecular biology · 2024
    Review
  6. Review
  7. Nucleolar stress: Friend or foe in cardiac function?Frontiers in cardiovascular medicine · 2022
    Review
  8. Cells · 2021
    Review
  9. The Feline Cardiomyopathies: 2. Hypertrophic cardiomyopathy.Journal of feline medicine and surgery · 2021
    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

8 authors at 2 institutions in 1 country.

Christian A TalloDepartment of Biological Sciences, North Carolina State University, Raleigh, NC 27695-7614, USA.
Laura H DuncanDepartment of Biological Sciences, North Carolina State University, Raleigh, NC 27695-7614, USA.
Akihiko H YamamotoThe Department of Entomology and Plant Pathology, North Carolina State University, Raleigh, NC 27695-7613, USA.
Joshua D SlaydonDepartment of Biological Sciences, North Carolina State University, Raleigh, NC 27695-7614, USA.
Gunjan H AryaDepartment of Biological Sciences, North Carolina State University, Raleigh, NC 27695-7614, USA.
Lavanya TurlapatiDepartment of Biological Sciences, North Carolina State University, Raleigh, NC 27695-7614, USA.
Trudy F C MackayThe Center for Human Genetics and Department of Genetics and Biochemistry, Clemson University, Greenwood, SC 29646, USA.
Mary A CarboneThe Comparative Medicine Institute, North Carolina State University, Raleigh, NC 27695, USA.
North Carolina State University · USCenter for Human Genetics · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

In cats, mutations in myosin binding protein C (encoded by the MYBPC3 gene) have been associated with hypertrophic cardiomyopathy (HCM). However, the molecular mechanisms linking these mutations to HCM remain unknown. Here, we establish Drosophila melanogaster as a model to understand this connection by generating flies harboring MYBPC3 missense mutations (A31P and R820W) associated with feline HCM. The A31P and R820W flies displayed cardiovascular defects in their heart rates and exercise endurance. We used RNA-seq to determine which processes are misregulated in the presence of mutant MYBPC3 alleles. Transcriptome analysis revealed significant downregulation of genes encoding small nucleolar RNA (snoRNAs) in exercised female flies harboring the mutant alleles compared to flies that harbor the wild-type allele. Other processes that were affected included the unfolded protein response and immune/defense responses. These data show that mutant MYBPC3 proteins have widespread effects on the transcriptome of co-regulated genes. Transcriptionally differentially expressed genes are also candidate genes for future evaluation as genetic modifiers of HCM as well as candidate genes for genotype by exercise environment interaction effects on the manifestation of HCM; in cats as well as humans.

Indexed as

Cardiomyopathy, HypertrophicRNA, Small NucleolarAnimalsCarrier ProteinsCatsDisease Models, AnimalDrosophilaDrosophila melanogasterFemaleHeat-Shock ProteinsMutationMyosin Binding Protein CCarrier ProteinsHeat-Shock ProteinsMyosin Binding Protein CRNA, Small NucleolarcMyBP-CDrosophila melanogasterfeline HCMhypertrophic cardiomyopathyMYBPC3

Identifiers

PMID33561224
PMCPMC7849908
OpenAlexW3119013074

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.