Regulation of chick dorsal root ganglion growth cone filopodia by protein kinase C

Bonsall, Joanna; Rehder, Vincent

doi:10.1016/s0006-8993(99)01725-4

Cited by 18 publications

(20 citation statements)

References 53 publications

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“…9). This result is consistent with findings previously reported for chick DRG neurons [Bonsall and Rehder, 1999], suggesting that the activity level of PKC may be important in regulating filopodial length in general. Filopodial length is likely determined by several factors, such as actin polymerization and depolymerization at the plus and minus ends of microfilaments, myosin-based motor molecules controlling the retrograde flow of cytoskeletal elements, as well as attachment of the cytoskeleton to the extracellular growth substrate [Welch et al, 1997].…”

Section: Discussionsupporting

confidence: 93%

“…The fact that these specific inhibitors had an effect on the average number of filopodia on a growth cone, however, suggested that they were used in a physiologically effective concentration range. These findings are in agreement with recent studies on chick DRG neurons [Bonsall and Rehder, 1999] (Bonsall and Rehder, unpublished observations), in which inhibitors of MLCK, CaMKII, and PKA were found to affect filopodial number but not filopodial length.…”

Section: Discussionsupporting

confidence: 93%

“…We have recently demonstrated that protein kinase C (PKC) activity is important in regulating filopodial behavior in chick dorsal root ganglion (DRG) neurons [Bonsall and Rehder, 1999]. Activation of PKC led to filopodial shortening, whereas inhibition of PKC caused filopodia to elongate.…”

Section: Introductionmentioning

confidence: 99%

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Filopodial behavior is dependent on the phosphorylation state of neuronal growth cones

Cheng

Mao

Rehder

2000

Cell Motil. Cytoskeleton

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Section: Discussionsupporting

confidence: 93%

Section: Discussionsupporting

confidence: 93%

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Filopodial behavior is dependent on the phosphorylation state of neuronal growth cones

Cheng

Mao

Rehder

2000

Cell Motil. Cytoskeleton

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“…There is evidence that the phosphorylation state of GAP-43 influences the organization of actin filaments in vari-ous growth cones (Meiri and Gordon-Weeks, 1990;Aigner and Caroni, 1993;He et al, 1997;Dent and Meiri, 1998;Lautermilch and Spitzer, 2000). We have shown previously in both chick DRG and Helisoma neurons that the activity of protein kinases, in particular PKC, acts as an important regulator of filopodial length (Bonsall and Rehder, 1999;Cheng et al, 2000). Inhibition of PKC caused filopodial elongation, whereas activation of PKC had the opposite effect, namely filopodial shortening.…”

Section: A Global Increase In Calcium Causes Filopodia To Elongatementioning

confidence: 89%

Local calcium changes regulate the length of growth cone filopodia

2002

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Previous studies have demonstrated that the free intracellular calcium concentration ([Ca(2+)](i)) in growth cones can act as an important regulator of growth cone behavior. Here we investigated whether there is a spatial and temporal correlation between [Ca(2+)](i) and one particular aspect of growth cone behavior, namely the regulation of growth cone filopodia. Calcium was released from the caged compound NP-EGTA (o-nitrophenyl EGTA tetrapotassium salt) to simulate a signaling event in the form of a transient increase in [Ca(2+)](i). In three different experimental paradigms, we released calcium either globally (within an entire growth cone), regionally (within a small area of the lamellipodium), or locally (within a single filopodium). We demonstrate that global photolysis of NP-EGTA in growth cones caused a transient increase in [Ca(2+)](i) throughout the growth cone and elicited subsequent filopodial elongation that was restricted to the stimulated growth cone. Pharmacological blockage of either calmodulin or the Ca(2+)-dependent phosphatase, calcineurin, inhibited the effect of uncaging calcium, suggesting that these enzymes are acting downstream of calcium. Regional uncaging of calcium in the lamellipodium caused a regional increase in [Ca(2+)](i), but induced filopodial elongation on the entire growth cone. Elevation of [Ca(2+)](i) locally within an individual filopodium resulted in the elongation of only the stimulated filopodium. These findings suggest that the effect of an elevation of [Ca(2+)](i) on filopodial behavior depends on the spatial distribution of the calcium signal. In particular, calcium signals within filopodia can cause filopodial length changes that are likely a first step towards directed filopodial steering events seen during pathfinding in vivo.

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“…Ligand-receptor interactions activate particular second messenger systems that cause directed changes in the growth cone's cytoskeleton [Gallo and Letourneau, 2000], which ultimately translate into growth cone steering events. Although there is a considerable body of knowledge describing the role of kinases on growth cone behavior [Bonsall and Rehder, 1999;Cheng et al, 2000;Jian et al, 1994] and neuronal guidance [Burden-Gulley et al, 1997;Jian et al, 1994;Fig. 5.…”

Section: Discussionmentioning

confidence: 99%

PLA₂ and secondary metabolites of arachidonic acid control filopodial behavior in neuronal growth cones

Geddis

Tornieri

Giesecke

et al. 2003

Cell Motil. Cytoskeleton

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The neuronal growth cone provides the sensory and motor structure that guides neuronal processes to their target. The ability of a growth cone to navigate correctly depends on its filopodia, which sample the environment by continually extending and retracting as the growth cone advances. Several second messengers systems that are activated upon contact with extracellular cues have been reported to affect growth cone morphology by changing the length and number of filopodia. Because recent studies have suggested that guidance cues can signal via G-protein coupled receptors to regulate phospholipases, we here investigated whether phospholipase A2 (PLA2) may control filopodial dynamics and could thereby affect neuronal pathfinding. Employing identified Helisoma neurons in vitro, we demonstrate that inhibition of PLA2 with 2 microM BPB caused a 40.3% increase in average filopodial length, as well as a 37.3% reduction in the number of filopodia on a growth cone. The effect of PLA2 inhibition on filopodial length was mimicked by the inhibition of G-proteins with 500 ng/ml pertussis toxin and was partially blocked by the simultaneous activation of PLA2 with 50 nM melittin. We provide evidence that PLA2 acts via production of arachidonic acid (AA), because (1) the effect of inhibition of PLA2 could be counteracted by supplying AA exogenously, and (2) the inhibition of cyclooxygenase, which metabolizes AA into prostaglandins, also increased filopodial length. We conclude that filopodial contact with extracellular signals that alter the activity of PLA2 can control growth cone morphology and may affect neuronal pathfinding by regulating the sensory radius of navigating growth cones.

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Regulation of chick dorsal root ganglion growth cone filopodia by protein kinase C

Cited by 18 publications

References 53 publications

Filopodial behavior is dependent on the phosphorylation state of neuronal growth cones

Filopodial behavior is dependent on the phosphorylation state of neuronal growth cones

Local calcium changes regulate the length of growth cone filopodia

PLA₂ and secondary metabolites of arachidonic acid control filopodial behavior in neuronal growth cones

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Regulation of chick dorsal root ganglion growth cone filopodia by protein kinase C

Cited by 18 publications

References 53 publications

Filopodial behavior is dependent on the phosphorylation state of neuronal growth cones

Filopodial behavior is dependent on the phosphorylation state of neuronal growth cones

Local calcium changes regulate the length of growth cone filopodia

PLA2 and secondary metabolites of arachidonic acid control filopodial behavior in neuronal growth cones

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Product

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PLA₂ and secondary metabolites of arachidonic acid control filopodial behavior in neuronal growth cones