BCL-2 DOES NOT CONTROL PROGRAMMED CELL DEATH IN THE IPLB-LdFB CELL LINE FROM THE INSECT LYMANTRIA DISPAR

Authors

  • Enzo Ottaviani,

    Corresponding author
    1. Department of Animal Biology, University of Modena and Reggio Emilia, Via campi 213/D, 41100, Modena, Italy
      To whom correspondence should be addressed: Prof. Enzo Ottaviani, Department of Animal Biology, Via Campi 213/D, 41100 Modena, Italy. Tel.: +059-205-5536; Fax: +059-205-5548; E-mail: ottaviani.enzo@unimo.it
    Search for more papers by this author
  • Davide Malagoli

    1. Department of Animal Biology, University of Modena and Reggio Emilia, Via campi 213/D, 41100, Modena, Italy
    Search for more papers by this author

To whom correspondence should be addressed: Prof. Enzo Ottaviani, Department of Animal Biology, Via Campi 213/D, 41100 Modena, Italy. Tel.: +059-205-5536; Fax: +059-205-5548; E-mail: ottaviani.enzo@unimo.it

Abstract

In the insect Lymantria dispar cell line IPLB-LdFB the presence of a Bcl-2-like molecule has been demonstrated. The Western blot analysis performed on the cells incubated with 2-deoxy-D-ribose (dRib), an apoptotic inducer, revealed that, in comparison with the control, the Bcl-2 expression was unaffected. Furthermore, incubation of the insect cells with an anti-Bcl-2 polyclonal antibody inhibited the apoptotic effect induced by dRib, and provoked mitochondrial membrane depolarization without any apoptotic phenomena. Similar behaviour was observed using the K+ ionophore valinomycin. From these findings, we hypothesize that the L. dispar Bcl-2-like protein is essential for maintenance of the mitochondrial membrane potential, but not, as usually thought, for the regulation of programmed cell death.

Ancillary