**4. Archetypes of single-cell repair: influence of injury type and cell type**

As previously stated, disruptions of the plasma membrane or cytoskeletal structures may lead to local or global increases in apparent membrane tension that prohibits spontaneous resealing to occur. Furthermore, plasma membrane damage can be accompanied by direct or indirect disruptions of the cytoskeleton, which worsen the damaged cell structural integrity. In contrast, plasma membrane disruptions generated by pore-forming toxins (PFTs) have little to no immediate impact on local in-plane membrane tension. As such, Ca2+-mediated exocytosis (see Section 4.1.2) and cytoskeletal remodeling (see Section 3.3) and cell-type (**Table 1**) may have profoundly different impacts depending on the type and size of the injury and may determine the healing pathway that is available to the cell (**Figure 2**) (reviewed in [35, 74]). Indeed, while uncontrolled entry of Ca2+ is a hallmark of all injury types, its intensity and distribution, together with the nature and size of the wound, as well as tissular context may control how the wound is repaired (**Figure 2**). The following section aims to present each wound-healing processes in the cellular context of which they were first identified. As it will become apparent in the next subsection, some processes, such as exocytosis, are quasi-ubiquitous, albeit with slight variations in vesicle species or molecular players involved. On the other hand, other processes, such as ESCRT-mediated membrane shedding (see Section 4.2.2) seem to be heavily dependent on wound size.



PFTs: Pore-forming toxins; ASM: Acid Sphingomyelinase

**Table 1.** Wound healing mechanisms according to cell-type.

How Plasma Membrane and Cytoskeletal Dynamics Influence Single-Cell Wound Healing: Mechanotransduction, Tension and Tensegrity http://dx.doi.org/10.5772/63765 201


**Figure 2.** Schematic (top) depicts lateral sections of the plasma membrane before and after different types of wounding (individual phospholipids represented as orange and beige heads with hairpin-like tails; cortical actin network represented as red lines; toxic pores represented in blue). Table (bottom) lists changes to wound-type-dependent factors of Ca2+ influx and tension, role of exocytosis and possible wound healing mechanisms upon different types of wounding. MCAs: membrane-to-cortex attachments; PFTs: pore-forming toxins.
