Introduction: brief historical overview.

Membranes are essential in defining the border and ensuring function of all living cells. As such they are vulnerable and have been a preferred target of attack throughout evolution. The most powerful way of damaging a membrane is through the insertion of pore-forming proteins. Research over the last decades shows that such proteins are produced by bacteria to attack bacterial or eukaryotic cells, vertebrates to kill invading organisms or infected cells, and by eukaryotic cells to "kill" mitochondria and trigger apoptosis. The breadth of effect of these proteins is bringing together, in a very exciting way, research communities that used to be unaware of each other.

Mechanistic effects of protein palmitoylation and the cellular consequences thereof.

S-palmitoylation involves the attachment of a 16-carbon long fatty acid chain to the cysteine residues of proteins. The process is enzymatic and dynamic with DHHC enzymes mediating palmitoylation and acyl-protein thioesterases reverting the reaction. Proteins that undergo this modification span almost all cellular functions. While the increase in hydrophobicity generated by palmitoylation has the obvious consequence of triggering membrane association, the effects on transmembrane proteins are less intuitive and span a vast range. We review here the current knowledge on palmitoylating and depalmitoylating enzymes, the methods that allow the study of this lipid modification and which drugs can affect it, and finally we focus on four cellular processes for which recent studies reveal an involvement of palmitoylation: endocytosis, reproduction and cell growth, fat and sugar homeostasis and signal transduction at the synapse.