Retrograde flow rate is increased in growth cones from myosin IIB knockout mice

Brown, Michael E.; Bridgman, Paul C.

doi:10.1242/jcs.00335

Cited by 92 publications

(73 citation statements)

References 34 publications

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“…This process reorganizes the cytoskeleton at synapses and is required for the stable expression of both long-term potentiation (LTP) and long-term contextual memory. In addition, we and others have found a rich diversity of functional Myosin II isoforms in dendritic spines (Brown and Bridgman 2003;Ryu et al 2006;Rubio et al 2011). While these studies have demonstrated the importance of Myosin II motors in the hippocampus, it is unclear if Myosin II motors are required for plasticity and memory in other brain regions.…”

mentioning

confidence: 83%

Myosin II motor activity in the lateral amygdala is required for fear memory consolidation

Gavin¹,

Rubio²,

Young³

et al. 2011

Learn. Mem.

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Learning induces dynamic changes to the actin cytoskeleton that are required to support memory formation. However, the molecular mechanisms that mediate filamentous actin (F-actin) dynamics during learning and memory are poorly understood. Myosin II motors are highly expressed in actin-rich growth structures including dendritic spines, and we have recently shown that these molecular machines mobilize F-actin in response to synaptic stimulation and learning in the hippocampus. In this study, we report that Myosin II motors in the rat lateral amygdala (LA) are essential for fear memory formation. Pretraining infusions of the Myosin II inhibitor, blebbistatin (blebb), disrupted long term memory, while short term memory was unaffected. Interestingly, both post-training and pretesting infusions had no effect on memory formation, indicating that Myosin II motors operate during or shortly after learning to promote memory consolidation. These data support the idea that Myosin II motor-force generation is a general mechanism that supports memory consolidation in the mammalian CNS.

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mentioning

confidence: 83%

Myosin II motor activity in the lateral amygdala is required for fear memory consolidation

Gavin¹,

Rubio²,

Young³

et al. 2011

Learn. Mem.

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“…Acute inactivation of myosin IIB leads to reduced growth cone area and loss of lamellipodia (Diefenbach et al, 2002). A reduced growth cone area was also observed for neurons of myosin IIB knock-out mice, but no changes in filopodial extension or retraction were reported (Bridgman et al, 2001;Brown and Bridgman, 2003). Thus, although signaling downstream of ROCK can regulate both myosin II and ADF/ cofilin, it is unclear how ROCK is involved in regulating filopodial motility.…”

Section: Introductionmentioning

confidence: 94%

“…Lin et al (1996) showed that filopodial elongation is negatively regulated by myosin-driven retrograde F-actin flow. However, Diefenbach et al (2002) found that chromophore-assisted laser inactivation (CALI) of myosin II did not affect filopodial dynamics and growth cones from myosin IIB knock-out mice showed normal filopodial dynamics (Brown and Bridgman, 2003). Furthermore, neurons express two main isoforms of myosin II that may regulate distinct aspects of neuronal morphology .…”

Section: -D ( S)-(ϫ)-mentioning

confidence: 99%

Brain-Derived Neurotrophic Factor Regulation of Retinal Growth Cone Filopodial Dynamics Is Mediated through Actin Depolymerizing Factor/Cofilin

Gehler¹,

Shaw²,

Sarmiere³

et al. 2004

J. Neurosci.

112

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The molecular mechanisms by which neurotrophins regulate growth cone motility are not well understood. This study investigated the signaling involved in transducing BDNF-induced increases of filopodial dynamics. Our results indicate that BDNF regulates filopodial length and number through a Rho kinase-dependent mechanism. Additionally, actin depolymerizing factor (ADF)/cofilin activity is necessary and sufficient to transduce the effects of BDNF. Our data indicate that activation of ADF/cofilin mimics the effects of BDNF on filopodial dynamics, whereas ADF/cofilin inactivity blocks the effects of BDNF. Furthermore, BDNF promotes the activation of ADF/ cofilin by reducing the phosphorylation of ADF/cofilin. Although inhibition of myosin II also enhances filopodial length, our results indicate that BDNF signaling is independent of myosin II activity and that the two pathways result in additive effects on filopodial length. Thus, filopodial extension is regulated by at least two independent mechanisms. The BDNF-dependent pathway works via regulation of ADF/cofilin, independently of myosin II activity.

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“…In vertebrate growth cones, two isoforms of the heavy chain of nonmuscle myosin II seem to have different locations and functions (Brown and Bridgman, 2003a). MHCIIB is more peripheral and is required for axon outgrowth, whereas MHCIIA is central and is required for cell adhesion (Rochlin et al, 1995;Wylie et al, 1998;Bridgman et al, 2001;Wylie and Chantler, 2001;Brown and Bridgman, 2003b). Drosophila has only a single zip gene, which may perform both functions.…”

Section: Mbs Prevents Loss Of Photoreceptors From the Eye Disc Epithementioning

confidence: 99%

Excessive Myosin Activity inMbsMutants Causes Photoreceptor Movement Out of theDrosophilaEye Disc Epithelium

Lee

Treisman

2004

MBoC

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Neuronal cells must extend a motile growth cone while maintaining the cell body in its original position. In migrating cells, myosin contraction provides the driving force that pulls the rear of the cell toward the leading edge. We have characterized the function of myosin light chain phosphatase, which down-regulates myosin activity, in Drosophila photoreceptor neurons. Mutations in the gene encoding the myosin binding subunit of this enzyme cause photoreceptors to drop out of the eye disc epithelium and move toward and through the optic stalk. We show that this phenotype is due to excessive phosphorylation of the myosin regulatory light chain Spaghetti squash rather than another potential substrate, Moesin, and that it requires the nonmuscle myosin II heavy chain Zipper. Myosin binding subunit mutant cells continue to express apical epithelial markers and do not undergo ectopic apical constriction. In addition, mutant cells in the wing disc remain within the epithelium and differentiate abnormal wing hairs. We suggest that excessive myosin activity in photoreceptor neurons may pull the cell bodies toward the growth cones in a process resembling normal cell migration. INTRODUCTIONThe cytoskeleton plays a variety of roles during development, allowing cells to change their shape, adhesive properties, and motility (Jamora and Fuchs, 2002). Two critical components of the cytoskeleton are actin and nonmuscle myosin II. The contractile activity of actomyosin complexes has been implicated in cell migration, epithelial sheet movements, cytokinesis, axon outgrowth, and cell adhesion (Maciver, 1996;Jacinto et al., 2002;Dent and Gertler, 2003). During migration of several cell types, myosin activity is required to retract the rear of the cell (Ridley et al., 2003).Nonmuscle myosin II consists of a hexamer of two myosin heavy chains (MHC), two myosin light chains (MLC), and two myosin regulatory light chains (MRLC) (Korn and Hammer, 1988). Phosphorylation of key serine and threonine residues on MRLC stimulates the ATPase activity of MHC and promotes its assembly into filaments, leading to stress fiber contraction (Adelstein and Conti, 1975;Craig et al., 1983;Umemoto et al., 1989;Katoh et al., 2001). Mutations in the Drosophila orthologs of these myosin subunits have provided insight into the developmental functions of myosin II. Mutations in zipper (zip), which encodes MHC, cause defects in cytokinesis, closure of the dorsal embryonic epidermis over the amnioserosa, axon patterning, and myofibril formation (Zhao et al., 1988;Young et al., 1993;Bloor and Kiehart, 2001). spaghetti squash (sqh), encoding MRLC, is required for cytokinesis, oogenesis, and imaginal disc eversion (Karess et al., 1991;Wheatley et al., 1995;Edwards and Kiehart, 1996;Jordan and Karess, 1997).Actin-binding proteins of the ezrin, radixin, and moesin (ERM) family are thought to link transmembrane proteins to the actin cytoskeleton (Bretscher, 1999). ERM proteins are activated by phosphorylation of a conserved threonine residue, which inhibits associati...

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Retrograde flow rate is increased in growth cones from myosin IIB knockout mice

Cited by 92 publications

References 34 publications

Myosin II motor activity in the lateral amygdala is required for fear memory consolidation

Myosin II motor activity in the lateral amygdala is required for fear memory consolidation

Brain-Derived Neurotrophic Factor Regulation of Retinal Growth Cone Filopodial Dynamics Is Mediated through Actin Depolymerizing Factor/Cofilin

Excessive Myosin Activity inMbsMutants Causes Photoreceptor Movement Out of theDrosophilaEye Disc Epithelium

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