ArticleDevelopment (Cambridge, England)2014
Translocating myonuclei have distinct leading and lagging edges that require kinesin and dynein.
Article in Development (Cambridge, England), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.
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.
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.
Who cites it
36 citing papers in PubMed, 63 citations in OpenAlex.
- Active microtubule-actin cross-talk mediated by a nesprin-2G-kinesin complex.Science advances · 2025Article
- The myonuclear domain in adult skeletal muscle fibres: past, present and future.The Journal of physiology · 2023Review
- Nuclear movement in multinucleated cells.Development (Cambridge, England) · 2022Review
- Article
- Ensconsin-dependent changes in microtubule organization and LINC complex-dependent changes in nucleus-nucleus interactions result in quantitatively distinct myonuclear positioning defects.Molecular biology of the cell · 2021Article
- Muscle memory: myonuclear accretion, maintenance, morphology, and miRNA levels with training and detraining in adult mice.Journal of cachexia, sarcopenia and muscle · 2020Article
- Reverse-engineering forces responsible for dynamic clustering and spreading of multiple nuclei in developing muscle cells.Molecular biology of the cell · 2020Article
- Review
- Getting into Position: Nuclear Movement in Muscle Cells.Trends in cell biology · 2020Review
- Impairments in contractility and cytoskeletal organisation cause nuclear defects in nemaline myopathy.Acta neuropathologica · 2019Article
- Inositol hexakisphosphate kinase 3 promotes focal adhesion turnover via interactions with dynein intermediate chain 2.Proceedings of the National Academy of Sciences of the United States of America · 2019Article
- TheThe Journal of cell biology · 2019Article
- Evidence of induced muscle regeneration persists for years in the mouse.Muscle & nerve · 2018Article
- Mechanical principles of nuclear shaping and positioning.The Journal of cell biology · 2018Review
- Review
- Mechanotransduction via the LINC complex regulates DNA replication in myonuclei.The Journal of cell biology · 2018Article
- Mechanical positioning of multiple nuclei in muscle cells.PLoS computational biology · 2018Article
- The cytoplasmic dynein transport machinery and its many cargoes.Nature reviews. Molecular cell biology · 2018Review
- An RNAi based screen in Drosophila larvae identifies fascin as a regulator of myoblast fusion and myotendinous junction structure.Skeletal muscle · 2018Article
- Myotonic Dystrophy and Developmental Regulation of RNA Processing.Comprehensive Physiology · 2018Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Nuclei are precisely positioned within all cells, and mispositioned nuclei are a hallmark of many muscle diseases. Myonuclear positioning is dependent on Kinesin and Dynein, but interactions between these motor proteins and their mechanisms of action are unclear. We find that in developing Drosophila muscles, Dynein and Kinesin work together to move nuclei in a single direction by two separate mechanisms that are spatially segregated. First, the two motors work together in a sequential pathway that acts from the cell cortex at the muscle poles. This mechanism requires Kinesin-dependent localization of Dynein to cell cortex near the muscle pole. From this location Dynein can pull microtubule minus-ends and the attached myonuclei toward the muscle pole. Second, the motors exert forces directly on individual nuclei independently of the cortical pathway. However, the activities of the two motors on the nucleus are polarized relative to the direction of myonuclear translocation: Kinesin acts at the leading edge of the nucleus, whereas Dynein acts at the lagging edge of the nucleus. Consistent with the activities of Kinesin and Dynein being polarized on the nucleus, nuclei rarely change direction, and those that do, reorient to maintain the same leading edge. Conversely, nuclei in both Kinesin and Dynein mutant embryos change direction more often and do not maintain the same leading edge when changing directions. These data implicate Kinesin and Dynein in two distinct and independently regulated mechanisms of moving myonuclei, which together maximize the ability of myonuclei to achieve their proper localizations within the constraints imposed by embryonic development.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.