Evidence map›Paper›PMID 26929344›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2016

Inactivation of 3-hydroxybutyrate dehydrogenase 2 delays zebrafish erythroid maturation by conferring premature mitophagy.

Gangarao Davuluri, Ping Song, Zhuoming Liu, David Wald, Takuya F Sakaguchi, Michael R Green, L Devireddy

Abstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
–field-weighted citation impact
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

20 citing papers in PubMed.

  1. Article
  2. The endothelial scavenger receptorbioRxiv : the preprint server for biology · 2026
    Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Review
  8. Article
  9. Article
  10. Mitochondrial connections with immune system in Zebrafish.Fish and shellfish immunology reports · 2021
    Review
  11. Review
  12. Article
  13. Frontiers in cell and developmental biology · 2021
    Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Review
  19. Review
  20. Review
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

7 authors.

Gangarao DavuluriDepartment of Pathobiology, Cleveland Clinic Lerner College of Medicine, Cleveland, OH 44120;
Ping SongCase Comprehensive Cancer Center, Case Western Reserve University, Cleveland, OH 44106;
Zhuoming LiuCase Comprehensive Cancer Center, Case Western Reserve University, Cleveland, OH 44106;
David WaldDepartment of Pathology, Case Western Reserve University, Cleveland, OH 44120;
Takuya F SakaguchiDepartment of Stem Cell Biology and Regenerative Medicine, Cleveland Clinic Lerner Research Institute, Cleveland, OH 44120;
Michael R GreenDepartment of Molecular, Cell and Cancer Biology, University of Massachusetts Medical School, Worcester, MA 01604; Howard Hughes Medical Institute, University of Massachusetts Medical School, Worcester, MA 01604 michael.green@umassmed.edu lxd259@gmail.com.ORCID http://orcid.org/0000-0003-3017-3298
L DevireddyCase Comprehensive Cancer Center, Case Western Reserve University, Cleveland, OH 44106; michael.green@umassmed.edu lxd259@gmail.com.

Funding

Role of the Mammalian Siderophore in Cellular Iron Metabolism and ErythropoiesisR01DK081395 · NIDDK · CASE WESTERN RESERVE UNIVERSITY · PI DEVIREDDY, LAXMINARAYANA R · 2008 to 2012
$1.7M
Role of Lipocalin 24p3 in Apoptosis and LeukemiaK01CA113838 · NCI · UNIV OF MASSACHUSETTS MED SCH WORCESTER · PI DEVIREDDY, LAXMINARAYANA R · 2006 to 2010
$702k
Howard Hughes Medical InstituteNCI NIH HHS K01 CA113838NCI NIH HHS K01CA113838NIDDK NIH HHS R01 DK081395NIDDK NIH HHS R01DK081395
6 · The paper itself

Abstract

Mitochondria are the site of iron utilization, wherein imported iron is incorporated into heme or iron-sulfur clusters. Previously, we showed that a cytosolic siderophore, which resembles a bacterial siderophore, facilitates mitochondrial iron import in eukaryotes, including zebrafish. An evolutionarily conserved 3-hydroxy butyrate dehydrogenase, 3-hydroxy butyrate dehydrogenase 2 (Bdh2), catalyzes a rate-limiting step in the biogenesis of the eukaryotic siderophore. We found that inactivation of bdh2 in developing zebrafish embryo results in heme deficiency and delays erythroid maturation. The basis for this erythroid maturation defect is not known. Here we show that bdh2 inactivation results in mitochondrial dysfunction and triggers their degradation by mitophagy. Thus, mitochondria are prematurely lost in bdh2-inactivated erythrocytes. Interestingly, bdh2-inactivated erythroid cells also exhibit genomic alterations as indicated by transcriptome analysis. Reestablishment of bdh2 restores mitochondrial function, prevents premature mitochondrial degradation, promotes erythroid development, and reverses altered gene expression. Thus, mitochondrial communication with the nucleus is critical for erythroid development.

Indexed as

AnimalsAutophagyEmbryo, NonmammalianErythrocytesGene Expression Regulation, DevelopmentalGene SilencingHydroxybutyrate DehydrogenaseMitochondriaMitophagyOxygenZebrafishZebrafish ProteinsBdh2 protein, zebrafishHydroxybutyrate DehydrogenaseOxygenZebrafish Proteins2,5-DHBAbdh2erythroid maturationmitophagyretrograde signaling

Identifiers

PMID26929344
PMCPMC4801243

What OpenQuestion holds

Textmetadata
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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.