article · 01/08/2004
Conditional beta 1-integrin gene deletion in neural crest cells causes severe developmental alterations of the peripheral nervous system
Résumé
Integrins are transmembrane receptors that are known to interact with the extracellular matrix and to be required for migration, proliferation, differentiation and apoptosis. We have generated mice with a neural crest cell-specific deletion of the beta1-integrin gene to analyse the role of beta1-integrins in neural crest cell migration and differentiation. This targeted mutation caused death within a month of birth. The loss of beta1-integrins from the embryo delayed the migration of Schwann cells along axons and induced multiple defects in spinal nerve arborisation and morphology. There was an almost complete absence of Schwann cells and sensory axon segregation and defective maturation in neuromuscular synaptogenesis. Thus, beta1-integrins are important for the control of embryonic and postnatal peripheral nervous system development.
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Pietri, T., Eder, O., Breau, M., Topilko, P., Blanche, M., Brakebusch, C., Fassler, R., Thiery, J., & Dufour, S. (2004). Conditional beta 1-integrin gene deletion in neural crest cells causes severe developmental alterations of the peripheral nervous system. Development, 131(16). https://doi.org/10.1242/dev.01264@article{Pietri2004_257,
author = {Pietri, T and Eder, O and Breau, MA and Topilko, P and Blanche, M and Brakebusch, C and Fassler, R and Thiery, JP and Dufour, S},
year = {2004},
month = {8},
title = {Conditional beta 1-integrin gene deletion in neural crest cells causes severe developmental alterations of the peripheral nervous system},
journal = {Development},
publisher = {COMPANY OF BIOLOGISTS LTD},
volume = {131},
number = {16},
address = {BIDDER BUILDING CAMBRIDGE COMMERCIAL PARK COWLEY RD, CAMBRIDGE CB4 4DL, CAMBS, ENGLAND},
abstract = {Integrins are transmembrane receptors that are known to interact with the extracellular matrix and to be required for migration, proliferation, differentiation and apoptosis. We have generated mice with a neural crest cell-specific deletion of the beta1-integrin gene to analyse the role of beta1-integrins in neural crest cell migration and differentiation. This targeted mutation caused death within a month of birth. The loss of beta1-integrins from the embryo delayed the migration of Schwann cells along axons and induced multiple defects in spinal nerve arborisation and morphology. There was an almost complete absence of Schwann cells and sensory axon segregation and defective maturation in neuromuscular synaptogenesis. Thus, beta1-integrins are important for the control of embryonic and postnatal peripheral nervous system development.},
url = {http://www.dx.doi.org/10.1242/dev.01264},
doi = {10.1242/dev.01264},
issn = {0950-1991},
}TY - JOUR
AU - Pietri, T
AU - Eder, O
AU - Breau, MA
AU - Topilko, P
AU - Blanche, M
AU - Brakebusch, C
AU - Fassler, R
AU - Thiery, JP
AU - Dufour, S
PY - 2004
DA - 2004/08/01
TI - Conditional beta 1-integrin gene deletion in neural crest cells causes severe developmental alterations of the peripheral nervous system
JO - Development
VL - 131
IS - 16
PB - COMPANY OF BIOLOGISTS LTD
SN - 0950-1991
AB - Integrins are transmembrane receptors that are known to interact with the extracellular matrix and to be required for migration, proliferation, differentiation and apoptosis. We have generated mice with a neural crest cell-specific deletion of the beta1-integrin gene to analyse the role of beta1-integrins in neural crest cell migration and differentiation. This targeted mutation caused death within a month of birth. The loss of beta1-integrins from the embryo delayed the migration of Schwann cells along axons and induced multiple defects in spinal nerve arborisation and morphology. There was an almost complete absence of Schwann cells and sensory axon segregation and defective maturation in neuromuscular synaptogenesis. Thus, beta1-integrins are important for the control of embryonic and postnatal peripheral nervous system development.
DO - 10.1242/dev.01264
UR - http://www.dx.doi.org/10.1242/dev.01264
ER -