Title

Transient alterations in granule cell proliferation, apoptosis and migration in postnatal developing cerebellum of CRMP1(-/-) mice

Authors

Authors

E. Charrier; B. Mosinger; C. Meissirel; M. Aguera; V. Rogemond; S. Reibel; P. Salin; N. Chounlamountri; V. Perrot; M. F. Belin; Y. Goshima; J. Honnorat; N. Thomasset;P. Kolattukudy

Comments

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Abbreviated Journal Title

Genes Cells

Keywords

RESPONSE MEDIATOR PROTEIN-2; ALZHEIMERS-DISEASE; NEURONAL MIGRATION; NERVOUS-SYSTEM; AXON GUIDANCE; COLLAPSIN; INVOLVEMENT; EXPRESSION; BRAIN; IDENTIFICATION; Cell Biology; Genetics & Heredity

Abstract

Collapsin response mediator proteins (CRMPs) consist of five homologous cytosolic proteins that participate in signal transduction involved in a variety of physiological events. CRMP1 is highly expressed during brain development; however, its functions remains unclear. To gain insight into its function, we generated CRMP1(-/-) mice with a knock-in LacZ gene. No gross anatomical changes or behavioral alterations were observed. Expression of CRMP1 was examined by the expression of the knocked-in LacZ gene, in situ hybridization with riboprobes and by imunohistochemistry. CRMP1 was found to be highly expressed in the developing the cerebellum, olfactory bulbs, hypothalamus and retina. In adults, expression level was high in the olfactory bulbs and hippocampus but very low in the retina and cerebellum and undetectable in hypothalamus. To study potential roles of CRMP1, we focused on cerebellum development. CRMP1(-/-) mice showed a decrease in the number of granule cells migrating out of explants of developing cerebellum, as did treatment of the explants from normal mice with anti-CRMP1 specific antibodies. CRMP1(-/-) mice showed a decrease in granule cell proliferation and apoptosis in external granule cell layers in vivo. Adult cerebellum of CRMP1(-/-) did not show any abnormalities.

Journal Title

Genes to Cells

Volume

11

Issue/Number

12

Publication Date

1-1-2006

Document Type

Article

Language

English

First Page

1337

Last Page

1352

WOS Identifier

WOS:000242195800002

ISSN

1356-9597

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