As we have shown here, overexpression of either lytM or ssaA restored cell viability, but only partially compensated cell morphology in the absence of WalKR, with a cell separation defect and abnormal, incomplete or misplaced division septa still present (Fig. 5).
On the other hand, the rostral increase in proliferation could be a mechanism to compensate for cell death and to maintain cell numbers in the rostral DG.
In contrast, germ cells, stem cells and cancer cells have a mechanism of synthesizing telomere DNA repeats to compensate the cell division-dependent telomere attrition, thereby bypassing the replicative senescence and being capable of self-replicating indefinitely [ 2].
At the same time, while hepatocytes and other intrinsic liver cells are stimulated to proliferate to compensate for cell loss, TGFβ is one of the signals that limit the proliferation of regenerating hepatocytes [ 4].
Extensive proliferation of progenitor cells in the intestinal crypts and their differentiation into mature epithelial cells continuously compensates for cell loss at the villus tip by anoikis.
In response to liver injury, mature hepatocytes proliferate to compensate for cell loss, and tissue resident progenitors also emerge and participate in the regenerative process (Fig. 2).
One possible explanation for this phenomenon is that apoptosis can promote proliferation critically needed to compensate for cell loss, for example, upon therapy, and to restore tissue homeostasis.
The compensatory mechanisms are complex and not fully understood, but are likely to involve adaptations within the surviving DAergic neurons, such as increased synthesis, metabolism and release of DA, to compensate for cell loss.
