Cell wound repair in <i>Drosophila</i> occurs through three distinct phases of membrane and cytoskeletal remodeling

Abreu-Blanco, María Teresa; Verboon, Jeffrey M.; Parkhurst, Susan M.

doi:10.1083/jcb.201011018

Cited by 134 publications

(204 citation statements)

References 36 publications

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“…4 b, red curve), which was further suppressed by preincubation with the Rho kinase inhibitor Y27632 (Fig. 4 b, green curve), a compound known to abrogate purse string formation (Abreu-Blanco et al, 2011). Interestingly, Y27632 prolonged sheet motion after hypotonic but not isotonic injury (Fig.…”

Section: Environmental Hypotonicity Triggers Migration Of Basal Epithmentioning

confidence: 99%

Osmotic surveillance mediates rapid wound closure through nucleotide release

Gault¹,

Enyedi²,

Niethammer³

2014

J Gen Physiol

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Section: Environmental Hypotonicity Triggers Migration Of Basal Epithmentioning

confidence: 99%

Osmotic surveillance mediates rapid wound closure through nucleotide release

Gault¹,

Enyedi²,

Niethammer³

2014

J Gen Physiol

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“…The cortical actin causes membrane tension, which prevents spontaneous resealing upon injury. 37 Ca 2C influx at the injury site triggers depolymerization of cortical actin as observed in Xenopus oocytes and Drosophila Embryos, 38 which is followed by resynthesis of the cortical actin. This progresses in way of a contractile actomyosin ring that forms a "purse string" -a circular structure and constricts circumferentially, in a manner coincident with the recruitment of filamentous actin (F-actin) and myosin-II at the wound borders.…”

Section: The Membrane Repair Machinerymentioning

confidence: 99%

“…39 PMR in Drosophila embryos also involves formation of actomyosin complex and a plasma membrane plug that is rapidly recruited from the surrounding edges of the membrane. 38 Additionally, intracellular vesicles are recruited to the wound perimeter enabling formation of a membrane patch within the actin ring to seal the wound.…”

Section: The Membrane Repair Machinerymentioning

confidence: 99%

S100 and annexin proteins identify cell membrane damage as the Achilles heel of metastatic cancer cells

Jaiswal

Nylandsted

2015

Cell Cycle

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“…Membrane resealing is a conserved process by which cells are able to survive mechanical disruption of the plasma membrane (14)(15)(16)(17)(18)(19). Dysferlin-null skeletal and cardiac muscle show enhanced uptake of membrane impermeable dye following laser-induced wounding, suggesting that dysferlin may play a role in membrane resealing (3,20).…”

Section: Introductionmentioning

confidence: 99%

Membrane damage-induced vesicle–vesicle fusion of dysferlin-containing vesicles in muscle cells requires microtubules and kinesin

McDade

Michele

2013

Human Molecular Genetics

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Mutations in the dysferlin gene resulting in dysferlin-deficiency lead to limb-girdle muscular dystrophy 2B and Myoshi myopathy in humans. Dysferlin has been proposed as a critical regulator of vesicle-mediated membrane resealing in muscle fibers, and localizes to muscle fiber wounds following sarcolemma damage. Studies in fibroblasts and urchin eggs suggest that trafficking and fusion of intracellular vesicles with the plasma membrane during resealing requires the intracellular cytoskeleton. However, the contribution of dysferlin-containing vesicles to resealing in muscle and the role of the cytoskeleton in regulating dysferlin-containing vesicle biology is unclear. Here, we use live-cell imaging to examine the behavior of dysferlin-containing vesicles following cellular wounding in muscle cells and examine the role of microtubules and kinesin in dysferlin-containing vesicle behavior following wounding. Our data indicate that dysferlin-containing vesicles move along microtubules via the kinesin motor KIF5B in muscle cells. Membrane wounding induces dysferlin-containing vesicle-vesicle fusion and the formation of extremely large cytoplasmic vesicles, and this response depends on both microtubules and functional KIF5B. In non-muscle cell types, lysosomes are critical mediators of membrane resealing, and our data indicate that dysferlincontaining vesicles are capable of fusing with lysosomes following wounding which may contribute to formation of large wound sealing vesicles in muscle cells. Overall, our data provide mechanistic evidence that microtubulebased transport of dysferlin-containing vesicles may be critical for resealing, and highlight a critical role for dysferlin-containing vesicle-vesicle and vesicle-organelle fusion in response to wounding in muscle cells.

show abstract

Cell wound repair in Drosophila occurs through three distinct phases of membrane and cytoskeletal remodeling

Abstract: Single-cell wound repair in Drosophila involves mechanistically distinct expansion, contraction, and closure phases.

Cited by 134 publications

References 36 publications

Osmotic surveillance mediates rapid wound closure through nucleotide release

Osmotic surveillance mediates rapid wound closure through nucleotide release

S100 and annexin proteins identify cell membrane damage as the Achilles heel of metastatic cancer cells

Membrane damage-induced vesicle–vesicle fusion of dysferlin-containing vesicles in muscle cells requires microtubules and kinesin

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