To most of us, it would seem intuitively unlikely that the strategies adopted by cells to ensure survival are mechanistically linked to the processes involved in cell death. However, the study of autophagy has revealed that this might well be the case, and this paradox is only one of the many interesting concepts to have emerged from research in this field.

In their Review article on page 439, Julian Lum, Ralph DeBerardinis and Craig Thompson outline the experimental evidence that has identified autophagy as a cross-species survival response to nutrient deprivation. They discuss the diverse physiological functions that are associated with autophagy and focus on the interplay between growth factor signalling — particularly through the Akt–Tor pathway — and the autophagic programme.

Despite evidence in support of its life-sustaining function, morphological changes in dying cells have implicated the autophagic machinery in the so-called type II, or autophagic, cell-death pathway. Furthermore, the induction of this cell-death pathway is inhibited by silencing the autophagy genes Atg6 and Atg7, and apoptosis-resistant mouse embryonic fibroblasts show cell death that is Atg5 and Atg6 dependent. In the Opinion article on page 505, Eric Baehrecke discusses how we might reconcile the involvement of a cell-survival pathway in the cell-death programme and he identifies the possible molecular mechanisms that might implement this dual role.

For the 'die-hard' sceptics, Baehrecke cites recent studies showing that the caspases — notorious cell-death executioners — also function in differentiation and proliferative events. In light of this, the role of autophagy in the cell's demise does not seem so incongruous. As the debate continues, one fact remains certain — nothing is ever simple in 'matters of life and death'.