Concerted actions of distinct nonmuscle myosin II isoforms drive intracellular membrane remodeling in live animals

Milberg, Oleg; Shitara, Akiko; Ebrahim, Seham; Masedunskas, Andrius; Tora, Muhibullah S; Tran, Duy T.; Chen, Yun; Conti, Mary Anne; Adelstein, Robert S.; Hagen, Karl S.; Weigert, Roberto

doi:10.1083/jcb.201612126

Cited by 48 publications

(74 citation statements)

References 61 publications

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“…The mT/mGFP probe provides a marker for both Cre expression and visualization of the plasma membrane (PM), as previously described (Masedunskas et al, 2011a;Milberg et al, 2017). Cre expression was induced in 5-10% of the acinar cells by the injection of a Cre-expressing adenovirus (Adeno-Cre) into the submandibular main duct (Milberg et al, 2017;Sramkova et al, 2009). In Cdc42 fl/fl-mT/mG mice, 3-4 weeks after the adenovirus injection, Cre-expressing cells exhibited large vacuolar structures labeled with membrane-targeted GFP (mGFP) and contiguous to the APM (Fig.…”

Section: Cdc42-depletion Causes the Expansion Of The Intercellular Camentioning

confidence: 99%

Cdc42 negatively regulates endocytosis during apical plasma membrane maintenance and development in mouse tubular organs in vivo

Shitara

Malec

Ebrahim

et al. 2018

Preprint

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Lumen establishment and maintenance are fundamental for tubular organs physiological functions. Most of the studies investigating the mechanisms regulating this process have been carried out in cell cultures or in smaller organisms, whereas little has been done in mammalian model systems in vivo. Here we used the salivary glands of live mice to examine the role of the small GTPase Cdc42 in the regulation of the homeostasis of the intercellular canaliculi, a specialized apical domain of the acinar cells, where protein and fluid secretion occur. Depletion of Cdc42 in adult mice induced a significant expansion of the apical canaliculi, whereas depletion at late embryonic stages resulted in a complete inhibition of their post-natal formation. In addition, intravital subcellular microscopy revealed that reduced levels of Cdc42 affected membrane trafficking from and towards the plasma membrane, highlighting a novel role for Cdc42 in membrane remodeling through the negative regulation of selected endocytic pathways.

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Section: Cdc42-depletion Causes the Expansion Of The Intercellular Camentioning

confidence: 99%

Cdc42 negatively regulates endocytosis during apical plasma membrane maintenance and development in mouse tubular organs in vivo

Shitara

Malec

Ebrahim

et al. 2018

Preprint

Self Cite

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“…Roberto Weigert (National Institutes of Health, Bethesda, USA) examines mechanisms regulating membrane remodelling in live rodents by using a novel imaging approach called intravital subcellular microscopy (iSMIC). Weigert's group has recently shown that, in exocrine glands, an actomyosin complex is recruited on the membranes of large secretory granules in order to control their exocytosis (Milberg et al, 2017). At the meeting, Weigert presented exciting new data showing that SEPT2, SEPT6 and SEPT7 are also recruited on the secretory granules and form a lattice-like cage that is required to control the assembly of the actomyosin complex.…”

Section: Role Of Septins In Membrane Trafficking and Tissue Integritymentioning

confidence: 99%

Meeting report – shining light on septins

Caudron

Yadav

2018

Journal of Cell Science

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Septins are enigmatic proteins; they bind GTP and assemble together like molecular Lego blocks to form intracellular structures of varied shapes such as filaments, rings and gauzes. To shine light on the biological mysteries of septin proteins, leading experts in the field came together for the European Molecular Biology Organization (EMBO) workshop held from 8–11 October 2017 in Berlin. Organized by Helge Ewers (Freie Universität, Berlin, Germany) and Serge Mostowy (Imperial College, London, UK), the workshop convened at the Harnack-Haus, a historic hub of scientific discourse run by the Max Planck Society.

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“…Force generation by myosin II isoforms is fundamental to the function of all eukaryotic cells. In addition to the well-known role of myosin II in generating muscle contraction, nonmuscle myosin II (NMII) isoforms are responsible for generating the mechanical forces that power cell division, cell motility, membrane remodeling during endo/exocytosis and embryo morphogenesis (Betapudi, 2014;Chandrasekar et al, 2014;Milberg et al, 2017;Sellers, 2000;Vicente-Manzanares et al, 2009). Dysregulation of force generation by nonmuscle myosin II can result in or contribute to disease conditions that include muscular dystrophy, cardiomyopathy, and metastatic cancer (Sellers, 2000).…”

Section: Introductionmentioning

confidence: 99%

Myosin II Tension Sensors Visualize Force Generation within the Actin Cytoskeleton in Living Cells

Rg¹,

Kota

et al. 2019

Preprint

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Type II myosin motors generate cytoskeletal forces that are central to cell division, embryogenesis, muscle contraction, and many other cellular functions. However, at present there is no method that can directly measure the forces generated by myosins in living cells. Here we describe a Förster resonance energy transfer (FRET)based tension sensor that can measure forces generated by Nonmuscle Myosin IIB (NMIIB) in living cells with piconewton (pN) sensitivity. Fluorescence lifetime imaging microscopy (FLIM)-FRET measurements indicate that the forces generated by NMIIB exhibit significant spatial and temporal heterogeneity, with inferred tensions that vary widely in different regions of the cell. This initial report highlights the potential utility of myosin-based tension sensors in elucidating the roles of cytoskeletal contractility in a wide variety of contexts.

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Concerted actions of distinct nonmuscle myosin II isoforms drive intracellular membrane remodeling in live animals

Abstract: Using intravital subcellular microscopy, Milberg et al. show that distinct but coordinated activities of two different nonmuscle myosin II isoforms drive the integration of large secretory granules into the plasma membrane during regulated exocytosis in live mice.

Cited by 48 publications

References 61 publications

Cdc42 negatively regulates endocytosis during apical plasma membrane maintenance and development in mouse tubular organs in vivo

Cdc42 negatively regulates endocytosis during apical plasma membrane maintenance and development in mouse tubular organs in vivo

Meeting report – shining light on septins

Myosin II Tension Sensors Visualize Force Generation within the Actin Cytoskeleton in Living Cells

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