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Postnatal Schwann cell proliferation but not myelination is strictly and uniquely dependent on cyclin-dependent kinase 4 (cdk4).
Mol Cell Neurosci 2008; 37(3):519-27MC

Abstract

Peripheral myelin formation depends on axonal signals that tightly control proliferation and differentiation of the associated Schwann cells. Here we demonstrate that the molecular program controlling proliferation of Schwann cells switches at birth. We have analyzed the requirements for three members of the cyclin-dependent kinase (cdk) family in Schwann cells using cdk-deficient mice. Mice lacking cdk4 showed a drastic decrease in the proliferation rate of Schwann cells at postnatal days 2 and 5, but proliferation was unaffected at embryonic day 18. In contrast, ablation of cdk2 and cdk6 had no significant influence on postnatal Schwann cell proliferation. Taken together, these findings indicate that postnatal Schwann cell proliferation is uniquely controlled by cdk4. Despite the lack of the postnatal wave of Schwann cell proliferation, axons were normally myelinated in adult cdk4-deficient sciatic nerves. Following nerve injury, Schwann cells lacking cdk4 were unable to re-enter the cell cycle, while Schwann cells deficient in cdk2 or cdk6 displayed proliferation rates comparable to controls. We did not observe compensatory effects such as elevated cdk4 levels in uninjured or injured nerves of cdk2 or cdk6-deficient mice. Our data demonstrate that prenatal and postnatal Schwann cell proliferation are driven by distinct molecular cues, and that postnatal proliferation is not a prerequisite for the generation of Schwann cell numbers adequate for correct myelination.

Authors+Show Affiliations

Institute of Cell Biology, ETH Zurich, Zurich, Switzerland. suzana.atanasoski@unibas.chNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

18191580

Citation

Atanasoski, Suzana, et al. "Postnatal Schwann Cell Proliferation but Not Myelination Is Strictly and Uniquely Dependent On Cyclin-dependent Kinase 4 (cdk4)." Molecular and Cellular Neurosciences, vol. 37, no. 3, 2008, pp. 519-27.
Atanasoski S, Boentert M, De Ventura L, et al. Postnatal Schwann cell proliferation but not myelination is strictly and uniquely dependent on cyclin-dependent kinase 4 (cdk4). Mol Cell Neurosci. 2008;37(3):519-27.
Atanasoski, S., Boentert, M., De Ventura, L., Pohl, H., Baranek, C., Beier, K., ... Suter, U. (2008). Postnatal Schwann cell proliferation but not myelination is strictly and uniquely dependent on cyclin-dependent kinase 4 (cdk4). Molecular and Cellular Neurosciences, 37(3), pp. 519-27. doi:10.1016/j.mcn.2007.11.005.
Atanasoski S, et al. Postnatal Schwann Cell Proliferation but Not Myelination Is Strictly and Uniquely Dependent On Cyclin-dependent Kinase 4 (cdk4). Mol Cell Neurosci. 2008;37(3):519-27. PubMed PMID: 18191580.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Postnatal Schwann cell proliferation but not myelination is strictly and uniquely dependent on cyclin-dependent kinase 4 (cdk4). AU - Atanasoski,Suzana, AU - Boentert,Matthias, AU - De Ventura,Lukas, AU - Pohl,Hartmut, AU - Baranek,Constanze, AU - Beier,Konstantin, AU - Young,Peter, AU - Barbacid,Mariano, AU - Suter,Ueli, Y1 - 2007/11/24/ PY - 2007/04/16/received PY - 2007/10/28/revised PY - 2007/11/15/accepted PY - 2008/1/15/pubmed PY - 2008/4/11/medline PY - 2008/1/15/entrez SP - 519 EP - 27 JF - Molecular and cellular neurosciences JO - Mol. Cell. Neurosci. VL - 37 IS - 3 N2 - Peripheral myelin formation depends on axonal signals that tightly control proliferation and differentiation of the associated Schwann cells. Here we demonstrate that the molecular program controlling proliferation of Schwann cells switches at birth. We have analyzed the requirements for three members of the cyclin-dependent kinase (cdk) family in Schwann cells using cdk-deficient mice. Mice lacking cdk4 showed a drastic decrease in the proliferation rate of Schwann cells at postnatal days 2 and 5, but proliferation was unaffected at embryonic day 18. In contrast, ablation of cdk2 and cdk6 had no significant influence on postnatal Schwann cell proliferation. Taken together, these findings indicate that postnatal Schwann cell proliferation is uniquely controlled by cdk4. Despite the lack of the postnatal wave of Schwann cell proliferation, axons were normally myelinated in adult cdk4-deficient sciatic nerves. Following nerve injury, Schwann cells lacking cdk4 were unable to re-enter the cell cycle, while Schwann cells deficient in cdk2 or cdk6 displayed proliferation rates comparable to controls. We did not observe compensatory effects such as elevated cdk4 levels in uninjured or injured nerves of cdk2 or cdk6-deficient mice. Our data demonstrate that prenatal and postnatal Schwann cell proliferation are driven by distinct molecular cues, and that postnatal proliferation is not a prerequisite for the generation of Schwann cell numbers adequate for correct myelination. SN - 1095-9327 UR - https://www.unboundmedicine.com/medline/citation/18191580/Postnatal_Schwann_cell_proliferation_but_not_myelination_is_strictly_and_uniquely_dependent_on_cyclin_dependent_kinase_4__cdk4__ L2 - https://linkinghub.elsevier.com/retrieve/pii/S1044-7431(07)00268-0 DB - PRIME DP - Unbound Medicine ER -