Stathmin-deficient mice develop an age-dependent axonopathy of the central and peripheral nervous systems.


Journal Article

Stathmin is a cytosolic protein that binds tubulin and destabilizes cellular microtubules, an activity regulated by phosphorylation. Despite its abundant expression in the developing mammalian nervous system and despite its high degree of evolutionary conservation, stathmin-deficient mice do not exhibit a developmental phenotype.(1) Here we report that aging stathmin(-/-) mice develop an axonopathy of the central and peripheral nervous systems. The pathological hallmark of the early axonal lesions was a highly irregular axoplasm predominantly affecting large, heavily myelinated axons in motor tracts. As the lesions progressed, degeneration of axons, dysmyelination, and an unusual glial reaction were observed. At the functional level, electrophysiology recordings demonstrated a significant reduction of motor nerve conduction velocity in stathmin(-/-) mice. At the molecular level, increased gene expression of SCG 10-like protein, a stathmin-related gene with microtubule destabilizing activity, was detected in the central nervous system of aging stathmin(-/-) mice. Together, these findings suggest that stathmin plays an essential role in the maintenance of axonal integrity.

Full Text

Duke Authors

Cited Authors

  • Liedtke, W; Leman, EE; Fyffe, REW; Raine, CS; Schubart, UK

Published Date

  • February 2002

Published In

Volume / Issue

  • 160 / 2

Start / End Page

  • 469 - 480

PubMed ID

  • 11839567

Pubmed Central ID

  • 11839567

International Standard Serial Number (ISSN)

  • 0002-9440

Digital Object Identifier (DOI)

  • 10.1016/S0002-9440(10)64866-3


  • eng

Conference Location

  • United States