ArticleCurrent biology : CB2012
Par-1 controls myosin-II activity through myosin phosphatase to regulate border cell migration.
Article in Current biology : CB, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.
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Who cites it
40 citing papers in PubMed, 88 citations in OpenAlex.
- A screen for adherens junction proteins regulating collective cell migration and testis morphogenesis reveals important roles for the Rab GAP RN-tre and the kinase Par-1.Molecular biology of the cell · 2026Article
- Polarity protein Par3 deficiency promotes metastasis of bladder cancer via interaction of Ppp1r12c.Biology direct · 2026Article
- Cell deformations generated by stochastic actomyosin waves drive in vivo random-walk swimming migration.Journal of cell science · 2025Article
- Myosin VI is expressed in developing ovarian follicles inFrontiers in cell and developmental biology · 2025Article
- Actomyosin contraction in the follicular epithelium provides the major mechanical force for follicle rupture duringProceedings of the National Academy of Sciences of the United States of America · 2024Article
- Collective cell migration relies on PPP1R15-mediated regulation of the endoplasmic reticulum stress response.Current biology : CB · 2024Article
- Asymmetrical positioning of cell organelles reflects the cell chirality of mouse myoblast cells.APL bioengineering · 2024Article
- Transcriptome analysis reveals temporally regulated genetic networks during Drosophila border cell collective migration.BMC genomics · 2023Article
- Nuclear lamin facilitates collective border cell invasion into confined spaces in vivo.The Journal of cell biology · 2023Article
- Septins regulate border cell surface geometry, shape, and motility downstream of Rho in Drosophila.Developmental cell · 2023Article
- Specific prostaglandins are produced in the migratory cells and the surrounding substrate to promotebioRxiv : the preprint server for biology · 2023Article
- Specific prostaglandins are produced in the migratory cells and the surrounding substrate to promoteFrontiers in cell and developmental biology · 2023Article
- Two Rac1 pools integrate the direction and coordination of collective cell migration.Nature communications · 2022Article
- Live imaging of delamination in Drosophila shows epithelial cell motility and invasiveness are independently regulated.Scientific reports · 2022Article
- Border cell polarity and collective migration require the spliceosome component Cactin.The Journal of cell biology · 2022Article
- MARK2 regulates directed cell migration through modulation of myosin II contractility and focal adhesion organization.Current biology : CB · 2022Article
- Siwi cooperates with Par-1 kinase to resolve the autoinhibitory effect of Papi for Siwi-piRISC biogenesis.Nature communications · 2022Article
- RhoA/ROCK Signaling Regulates Drp1-Mediated Mitochondrial Fission During Collective Cell Migration.Frontiers in cell and developmental biology · 2022Article
- Fascin limits Myosin activity withineLife · 2021Article
- Germline soma communication mediated by gap junction proteins regulates epithelial morphogenesis.PLoS genetics · 2021Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
backgroundLocalized actomyosin contraction couples with actin polymerization and cell-matrix adhesion to regulate cell protrusions and retract trailing edges of migrating cells. Although many cells migrate in collective groups during tissue morphogenesis, mechanisms that coordinate actomyosin dynamics in collective cell migration are poorly understood. Migration of Drosophila border cells, a genetically tractable model for collective cell migration, requires nonmuscle myosin-II (Myo-II). How Myo-II specifically controls border cell migration and how Myo-II is itself regulated is largely unknown.
resultsWe show that Myo-II regulates two essential features of border cell migration: (1) initial detachment of the border cell cluster from the follicular epithelium and (2) the dynamics of cellular protrusions. We further demonstrate that the cell polarity protein Par-1 (MARK), a serine-threonine kinase, regulates the localization and activation of Myo-II in border cells. Par-1 binds to myosin phosphatase and phosphorylates it at a known inactivating site. Par-1 thus promotes phosphorylated myosin regulatory light chain, thereby increasing Myo-II activity. Furthermore, Par-1 localizes to and increases active Myo-II at the cluster rear to promote detachment; in the absence of Par-1, spatially distinct active Myo-II is lost.
conclusionsWe identify a critical new role for Par-1 kinase: spatiotemporal regulation of Myo-II activity within the border cell cluster through localized inhibition of myosin phosphatase. Polarity proteins such as Par-1, which intrinsically localize, can thus directly modulate the actomyosin dynamics required for border cell detachment and migration. Such a link between polarity proteins and cytoskeletal dynamics may also occur in other collective cell migrations.
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