Transfection of S2R+ drosophila cells using Flyfectin

S2R+ cells cultured in Schneider's medium with 5% FBS were transfected using Flyfectin.

This paper shows the efficiency of Flyfectin to transfect S2R+ insect cells.

article reference: J Cell Biol. 2014 Feb 3;204(3):303-12. 

Reduction of endoplasmic reticulum stress attenuates the defects caused by Drosophila mitofusin depletion.

Debattisti V, Pendin D, Ziviani E, Daga A, Scorrano L.

Abstract

Ablation of the mitochondrial fusion and endoplasmic reticulum (ER)-tethering protein Mfn2 causes ER stress, but whether this is just an epiphenomenon of mitochondrial dysfunction or a contributor to the phenotypes in mitofusin (Mfn)-depleted Drosophila melanogaster is unclear. In this paper, we show that reduction of ER dysfunction ameliorates the functional and developmental defects of flies lacking the single Mfn mitochondrial assembly regulatory factor (Marf). Ubiquitous or neuron- and muscle-specific Marf ablation was lethal, altering mitochondrial and ER morphology and triggering ER stress that was conversely absent in flies lacking the fusion protein optic atrophy 1. Expression of Mfn2 and ER stress reduction in flies lacking Marf corrected ER shape, attenuating the developmental and motor defects. Thus, ER stress is a targetable pathogenetic component of the phenotypes caused by Drosophila Mfn ablation.

FlyFectin™ from OZ Biosciences is a powerful reagent specifically designed to obtain highly efficient and reproducible transfection of insect cells. It is adapted to the delivery of all types of nucleic acids. FlyFectin™ can be used for many applications including for the production of recombinant protein using Baculovirus expression system