Evidence map›Paper›PMID 36882085›Full record

ArticleNucleic acids research2023

Dynamic interplay between RPL3- and RPL3L-containing ribosomes modulates mitochondrial activity in the mammalian heart.

Ivan Milenkovic, Helaine Graziele Santos Vieira, Morghan C Lucas, Jorge Ruiz-Orera, Giannino Patone, Scott Kesteven, Jianxin Wu, Michael Feneley, Guadalupe Espadas, Eduard Sabidó and 4 more

Open access · goldAbstract read
In one paragraph

Article in Nucleic acids research, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed
7.7field-weighted citation impact, top 2% 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

38 citing papers in PubMed, 50 citations in OpenAlex.

  1. METTL18 is Required for Developmental, Metabolic, and Endocrine Regulation of Mammalian Growth.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026
    Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Chromatin topology control by a muscle-specific ribosomal protein.bioRxiv : the preprint server for biology · 2026
    Article
  7. Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Review
  14. Understanding inherited cardiomyopathies: clinical aspects and genetic determinants.Medizinische Genetik : Mitteilungsblatt des Berufsverbandes Medizinische Genetik e.V · 2025
    Article
  15. Review
  16. Article
  17. Article
  18. Ribosomal protein paralogues in ribosome specialization.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2025
    Review
  19. Specialized ribosomes: integrating new insights and current challenges.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2025
    Review
  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

14 authors at 6 institutions in 4 countries.

Ivan MilenkovicCentre for Genomic Regulation (CRG), The Barcelona Institute of Science and Technology, Dr. Aiguader 88, Barcelona 08003, Spain.
Helaine Graziele Santos VieiraCentre for Genomic Regulation (CRG), The Barcelona Institute of Science and Technology, Dr. Aiguader 88, Barcelona 08003, Spain.ORCID 0000-0002-1114-9439
Morghan C LucasCentre for Genomic Regulation (CRG), The Barcelona Institute of Science and Technology, Dr. Aiguader 88, Barcelona 08003, Spain.
Jorge Ruiz-OreraCardiovascular and Metabolic Sciences, Max Delbrück Center for Molecular Medicine in the Helmholtz Association (MDC), D-13125 Berlin, Germany.
Giannino PatoneCardiovascular and Metabolic Sciences, Max Delbrück Center for Molecular Medicine in the Helmholtz Association (MDC), D-13125 Berlin, Germany.
Scott KestevenVictor Chang Cardiac Research Institute, Darlinghurst, NSW 2010, Australia.
Jianxin WuVictor Chang Cardiac Research Institute, Darlinghurst, NSW 2010, Australia.
Michael FeneleyVictor Chang Cardiac Research Institute, Darlinghurst, NSW 2010, Australia.
Guadalupe EspadasCentre for Genomic Regulation (CRG), The Barcelona Institute of Science and Technology, Dr. Aiguader 88, Barcelona 08003, Spain.
Eduard SabidóCentre for Genomic Regulation (CRG), The Barcelona Institute of Science and Technology, Dr. Aiguader 88, Barcelona 08003, Spain.
Norbert HübnerCardiovascular and Metabolic Sciences, Max Delbrück Center for Molecular Medicine in the Helmholtz Association (MDC), D-13125 Berlin, Germany.
Sebastiaan van HeeschPrincess Máxima Center for Pediatric Oncology, Heidelberglaan 25, 3584 CS, Utrecht, The Netherlands.ORCID 0000-0001-9593-1980
Mirko VölkersUniversity of Heidelberg, Heidelberg, Germany.ORCID 0000-0003-2344-1856
Eva Maria NovoaCentre for Genomic Regulation (CRG), The Barcelona Institute of Science and Technology, Dr. Aiguader 88, Barcelona 08003, Spain.ORCID 0000-0002-9367-6311
Universitat Pompeu Fabra · ESMax Delbrück Center · DEVictor Chang Cardiac Research Institute · AUCentre for Genomic Regulation · ESHeidelberg University · DEPrincess Máxima Center · NL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The existence of naturally occurring ribosome heterogeneity is now a well-acknowledged phenomenon. However, whether this heterogeneity leads to functionally diverse 'specialized ribosomes' is still a controversial topic. Here, we explore the biological function of RPL3L (uL3L), a ribosomal protein (RP) paralogue of RPL3 (uL3) that is exclusively expressed in skeletal muscle and heart tissues, by generating a viable homozygous Rpl3l knockout mouse strain. We identify a rescue mechanism in which, upon RPL3L depletion, RPL3 becomes up-regulated, yielding RPL3-containing ribosomes instead of RPL3L-containing ribosomes that are typically found in cardiomyocytes. Using both ribosome profiling (Ribo-seq) and a novel orthogonal approach consisting of ribosome pulldown coupled to nanopore sequencing (Nano-TRAP), we find that RPL3L modulates neither translational efficiency nor ribosome affinity towards a specific subset of transcripts. In contrast, we show that depletion of RPL3L leads to increased ribosome-mitochondria interactions in cardiomyocytes, which is accompanied by a significant increase in ATP levels, potentially as a result of fine-tuning of mitochondrial activity. Our results demonstrate that the existence of tissue-specific RP paralogues does not necessarily lead to enhanced translation of specific transcripts or modulation of translational output. Instead, we reveal a complex cellular scenario in which RPL3L modulates the expression of RPL3, which in turn affects ribosomal subcellular localization and, ultimately, mitochondrial activity.

Indexed as

HeartMitochondriaRibosomal ProteinsRibosomesAnimalsMiceMuscle, SkeletalPleckstrin Homology DomainsProtein BiosynthesisRibosomal Protein L3PLEKHM2 protein, humanRibosomal Protein L3Ribosomal ProteinsRpl3 protein, mouse

Identifiers

PMID36882085
PMCPMC10287911
OpenAlexW4323349882

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.