No abstract

KIF3A, KIF3B and KIF3C are kinesin-related motor subunits of the KIF3 family that associate to form the kinesin-II motor complex in which KIF3C and KIF3B are alternative partners of KIF3A. We have analysed the expression of Kif3 mRNAs during prenatal murine development. Kif3c transcripts are detectable from embryonic day 12.5 and persist throughout development both in the CNS and in some peripheral ganglia.Comparison of the expression patterns of the Kif3 genes revealed that Kif3c and Kif3a mRNAs colocalize in the CNS, while only Kif3a is also present outside the CNS. In contrast, Kif3b is detectable in several non-neural tissues. We have also performed immunocytochemical analyses of the developing rat brain and have found the presence of the KIF3C protein in selected brain regions and in several ®bre systems. Using neuroblastoma cells as an in vitro model for neuronal differentiation, we found that retinoic acid stimulated the expression of the three Kif3 and the kinesin-associated protein genes, although with different time courses. The selective expression of Kif3c in the nervous system during embryonic development and its up-regulation during neuroblastoma differentiation suggest a role for this motor during maturation of neuronal cells.

fesce.riccardo@hsr.it

The growth of hepatoma cells can be inhibited by treatment with TGFb1 or with exogenous reducing agents. To gain information on the molecular mechanisms underlying growth arrest, we visualized and compared gene expression pro®les of proliferating versus non proliferating HepG2 cells by computer-assisted gene ®shing, an improved technique of RNA ®ngerprinting that allows the selective ampli®cation of coding regions within transcripts. While many transcripts are selectively regulated by either treatment, a set of bands appear to be coordinately regulated by 2ME and TGFb1, suggesting their possible involvement in the mechanisms of growth arrest. Display tags corresponding to 18 di erentially expressed genes were cloned and, in most cases, identi®ed as known genes or, more frequently, as their homospeci®c/cross-speci®c homologues. A novel member of the kinesin superfamily was identi®ed amongst the genes induced by both 2ME and TGFb1. This gene, KIF3C, is upregulated in several cell lines undergoing growth arrest. Taken together, our ®ndings show that computer-assisted gene ®shing is a powerful tool for the identi®cation and cloning of genes involved in the control of cell proliferation and indicate that extracellular reducing agents can regulate cell growth through modulation of gene expression.