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On page 661, Lee et al. show that oligodendrocytes (OLs) get their branchy shape from a microtubule-assembling protein called CNP. Loss of CNP in OLs leads to axonal degeneration in enveloped neurons.Axons depend on myelination by glial cells such as OLs for the transmission of action potentials. The myelin sheath contains a large amount of 2'3'-cyclic nucleotide 3'-phosphodiesterase (CNP), but what this protein was doing in OLs was not known. The new results reveal that CNP is a tubulin-binding protein that allows cells to extend long branched processes.* J) p. O7 U3 T
4 S7 }; w6 O; C r2 g/ _' t% ~/ ?The authors find that CNP binds strongly to tubulin heterodimers. In vitro, CNP induces microtubule assembly and polymerizes along with the tubulin dimers. In cells, CNP rearranges both the microtubule and F-actin networks and induces the formation of processes, even in cells that normally do not express CNP.
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OLs expressing polymerization-defective CNP had fewer highly branched processes, which normally envelop axons. Mice mutant for CNP have been shown to develop structural defects near axon–OL junctions that eventually lead to axonal degeneration. Without CNP, these OLs probably lack the structural support system needed to maintain processes. The abnormal cytoskeleton might also disrupt protein transport essential for sustaining the axon–OL connection.(CNP (green) expression causes the elonga) |
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发表于 2009-3-6 08:55
发表于 2015-5-30 18:09
