Kif1Bβ isoform is enriched in motor neurons but does not change in a mouse model of amyotrophic lateral sclerosis

Laura Conforti, Carlotta Dell'Agnello, Novella Calvaresi, Massimo Tortarolo, Andrea Giorgini, Michael P. Coleman, Caterina Bendotti

Research output: Contribution to journalArticlepeer-review


The kinesin superfamily motor protein Kif1B is expressed in two isoforms, Kif1Bα and Kif1Bβ, with distinct cargo- binding domains. We examined the mRNA distribution of the two isoforms in adjacent sections of brain and spinal cord of adult mice using in situ hybridization analysis. Kif1Bβ mRNA is enriched in several regions of brain and spinal cord. Its levels are four to five times higher than that of the α isoform, which was barely detectable. The highest mRNA levels of Kif1Bβ were found in the cortex, hippocampus, cerebellum and the grey matter of the spinal cord. At the cellular level the highest signal was found in motor neurons in the motor nuclei of medulla oblongata and the ventral horn of spinal cord. Because expression of other Kif genes is altered in amyotrophic lateral sclerosis (ALS) models, we examined the expression level of Kif1Bβ mRNA in the spinal cord of transgenic mice carrying the SOD1G93A mutation, a model of familial ALS, at presymptomatic and early stages of the disease. No changes were observed in Kif1Bβ mRNA in motor neurons or in other regions of the spinal cord. These findings indicate that Kif1Bα, which modulates the transport of mitochondria, may play a major role in tissues other than the central nervous system. Instead Kif1Bβ, responsible for the transport of synaptic vesicle precursors, seems to play an important role in the nervous system, particularly in the lower motor neurons. The absence of changes of Kif1Bβ mRNA in transgenic SOD1G93A mice suggests that other molecular mechanisms may play a role in the disruption of axonal transport occurring in the motor neurons of these mice.

Original languageEnglish
Pages (from-to)732-739
Number of pages8
JournalJournal of Neuroscience Research
Issue number5
Publication statusPublished - Mar 1 2003


  • Axonal transport
  • In situ hybridization
  • Kinesin
  • Motor neuron disease
  • Transgenic mice

ASJC Scopus subject areas

  • Neuroscience(all)


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