 |
Previous Article | Next Article 
The Journal of Neuroscience, February 1, 1998, 18(3):987-998
Arginine Kinase Expression and Localization in Growth Cone
Migration
Yu-mei E.
Wang,
Pia
Esbensen, and
David
Bentley
Neurobiology Division, Department of Molecular and Cell Biology,
University of California, Berkeley, California 94720-3200
Migrating neuronal growth cones exert traction forces that are
generated by ATP-driven F-actin/myosin interactions. Sustained generation of these forces may require an energy supply mediated by the
guanidino kinases, creatine kinase and arginine kinase. We cloned and
sequenced grasshopper arginine kinase and examined its expression
during embryogenesis and its subcellular localization in
vivo and in vitro. During the first half of
embryogenesis, arginine kinase is expressed selectively in a small
percentage of ectodermal cells (dorsal closure cells), in a small
percentage of mesodermal cells (muscle pioneers), and throughout the
developing CNS. Most of these cell types are motile, including nascent
neurons, muscle pioneers, dorsal closure cells, and many CNS glia.
Neuroblasts also strongly express arginine kinase; they are nonmotile
but are undergoing repeated rounds of (ATP-dependent) mitosis. Arginine kinase is colocalized with F-actin in a narrow band along the leading
edges of lamellipodia of migrating glia. In neurons undergoing axonogenesis, arginine kinase is concentrated in growth cones and
extends to the tips of filopodia. The amount of arginine kinase varies
widely between growth cones, even between different growth cones of the
same neuron. Energy for growth cone migration appears to be mobilized
by (1) selective expression of arginine kinase by neurons, (2)
localization of arginine kinase within growth cones, and (3)
concentration of arginine kinase within specific growth cones,
depending on the traction forces being generated. Mobilization of
guanidino kinases may participate in the selective growth of specific
growth cones.
Key words:
arginine kinase; creatine kinase; growth cone; cell
motility; axonogenesis; neurogenesis
Copyright © 1998 Society for Neuroscience 0270-6474/98/183987-12$05.00/0
This article has been cited by other articles:

|
 |

|
 |
 
R. S. O'Connor, C. M. Steeds, R. W. Wiseman, and G. K. Pavlath
Phosphocreatine as an energy source for actin cytoskeletal rearrangements during myoblast fusion
J. Physiol.,
June 15, 2008;
586(12):
2841 - 2853.
[Abstract]
[Full Text]
[PDF]
|
 |
|

|
 |

|
 |
 
O. Braissant, H. Henry, A.-M. Villard, M.-G. Zurich, M. Loup, B. Eilers, G. Parlascino, E. Matter, O. Boulat, P. Honegger, et al.
Ammonium-Induced Impairment of Axonal Growth Is Prevented through Glial Creatine
J. Neurosci.,
November 15, 2002;
22(22):
9810 - 9820.
[Abstract]
[Full Text]
[PDF]
|
 |
|

|
 |

|
 |
 
M. Binder, V. Mahler, B. Hayek, W. R. Sperr, M. Scholler, S. Prozell, G. Wiedermann, P. Valent, R. Valenta, and M. Duchene
Molecular and Immunological Characterization of Arginine Kinase from the Indianmeal Moth, Plodia interpunctella, a Novel Cross-Reactive Invertebrate Pan-Allergen
J. Immunol.,
November 1, 2001;
167(9):
5470 - 5477.
[Abstract]
[Full Text]
[PDF]
|
 |
|

|
 |

|
 |
 
V. B. Mahajan, K. S. Pai, A. Lau, and D. D. Cunningham
Creatine kinase, an ATP-generating enzyme, is required for thrombin receptor signaling to the cytoskeleton
PNAS,
October 24, 2000;
97(22):
12062 - 12067.
[Abstract]
[Full Text]
[PDF]
|
 |
|

|
 |

|
 |
 
M. Wyss and R. Kaddurah-Daouk
Creatine and Creatinine Metabolism
Physiol Rev,
July 1, 2000;
80(3):
1107 - 1213.
[Abstract]
[Full Text]
[PDF]
|
 |
|
|

|