Adult planarians are capable of undergoing regeneration and body remodelling in order to adapt to physical damage or extreme
environmental conditions. Moreover, most planarians can tolerate long periods of starvation and during this time, they shrink
from an adult size to, and sometimes beyond, the initial size at hatching. Indeed, these properties have made them a classic
model to study stem cells and regeneration. Under such stressful conditions, food reserves from the gastrodermis and parenchyma
are first used up and later the testes, copulatory organs and ovaries are digested. More surprisingly, when food is again
made available to shrunken individuals, they grow back to adult size and all their reproductive structures reappear. These
cycles of growth and shrinkage may occur over long periods without any apparent impairment to the individual, or to its future
maturation and breeding capacities. This plasticity resides in a mesoderm tissue known as the parenchyma, which is formed
by several differentiated non-proliferating cell types and only one mitotically active cell type, the neoblasts, which represent
approximately 20–30% of the cells in the parenchyma. Neoblasts are generally thought to be somatic stem-cells that participate
in the normal continuous turnover of all cell types in planarians. Hence, planarians are organisms that continuously adapt
their bodies (morphallaxis) to different environmental stresses (i.e.: injury or starvation). This adaptation involves a variety
of processes including proliferation, differentiation, apoptosis and autophagy, all of which are perfectly orchestrated and
tightly regulated to remodel or restore the body pattern. While neoblast biology and body re-patterning are currently the
subject of intense research, apoptosis and autophagy remain much less studied. In this review we will summarize our current
understanding and hypotheses regarding where and when apoptosis and autophagy occur and fulfil an essential role in planarians.
Keywords Planarian - Autophagy - Apoptosis - Cell death - Regeneration - Remodelling