Evidence map›Paper›PMID 20566368›Full record

ArticleDevelopmental biology2010

Nrk2b-mediated NAD+ production regulates cell adhesion and is required for muscle morphogenesis in vivo: Nrk2b and NAD+ in muscle morphogenesis.

Michelle F Goody, Meghan W Kelly, Kevin N Lessard, Andre Khalil, Clarissa A Henry

Abstract read
In one paragraph

Article in Developmental biology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.

0numbers the graph read from it
0cells of the map it votes in
42citing papers in PubMed
1.7field-weighted citation impact, top 18% 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

42 citing papers in PubMed, 69 citations in OpenAlex.

  1. Trial
  2. Myotendinous Junction development and repair.Journal of orthopaedic translation · 2026
    Review
  3. Article
  4. Review
  5. Article
  6. Article
  7. Article
  8. Axial segmentation by iterative mechanical signaling.bioRxiv : the preprint server for biology · 2023
    Article
  9. Balancing NADCellular and molecular life sciences : CMLS · 2022
    Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Zebrafish Models ofFrontiers in molecular neuroscience · 2020
    Article
  16. Article
  17. Review
  18. Article
  19. Review
  20. Ethanol Exposure Causes Muscle Degeneration in Zebrafish.Journal of developmental biology · 2018
    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

5 authors at 2 institutions in 1 country.

Michelle F GoodySchool of Biology and Ecology, University of Maine, Orono, ME 04469, USA.
Meghan W Kelly
Kevin N Lessard
Andre Khalil
Clarissa A Henry
University of Maine · USJackson Laboratory · US

Funding

Analysis of Myotome Boundary Morphogenesis During Zebrafish DevelopmentR01HD052934 · NICHD · UNIVERSITY OF MAINE ORONO · PI HENRY, CLARISSA A · 2007 to 2011
$1.4M
NICHD NIH HHS R01 HD052934
6 · The paper itself

Abstract

Cell-matrix adhesion complexes (CMACs) play fundamental roles during morphogenesis. Given the ubiquitous nature of CMACs and their roles in many cellular processes, one question is how specificity of CMAC function is modulated. The clearly defined cell behaviors that generate segmentally reiterated axial skeletal muscle during zebrafish development comprise an ideal system with which to investigate CMAC function during morphogenesis. We found that Nicotinamide riboside kinase 2b (Nrk2b) cell autonomously modulates the molecular composition of CMACs in vivo. Nrk2b is required for normal Laminin polymerization at the myotendinous junction (MTJ). In Nrk2b-deficient embryos, at MTJ loci where Laminin is not properly polymerized, muscle fibers elongate into adjacent myotomes and are abnormally long. In yeast and human cells, Nrk2 phosphorylates Nicotinamide Riboside and generates NAD+ through an alternative salvage pathway. Exogenous NAD+ treatment rescues MTJ development in Nrk2b-deficient embryos, but not in laminin mutant embryos. Both Nrk2b and Laminin are required for localization of Paxillin, but not beta-Dystroglycan, to CMACs at the MTJ. Overexpression of Paxillin in Nrk2b-deficient embryos is sufficient to rescue MTJ integrity. Taken together, these data show that Nrk2b plays a specific role in modulating subcellular localization of discrete CMAC components that in turn plays roles in musculoskeletal development. Furthermore, these data suggest that Nrk2b-mediated synthesis of NAD+ is functionally upstream of Laminin adhesion and Paxillin subcellular localization during MTJ development. These results indicate a previously unrecognized complexity to CMAC assembly in vivo and also elucidate a novel role for NAD+ during morphogenesis.

Indexed as

AnimalsCell AdhesionDystroglycansEmbryo, NonmammalianLamininMorphogenesisMuscle DevelopmentMusclesMuscle, SkeletalNADPaxillinPhosphotransferases (Alcohol Group Acceptor)TendonsZebrafishDystroglycansLamininNADnicotinamide riboside kinasePaxillinPhosphotransferases (Alcohol Group Acceptor)

Identifiers

PMID20566368
PMCPMC2917104
OpenAlexW1799344545

What OpenQuestion holds

Textmetadata
LicenceTDM
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.