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Cell wound repair in Drosophila occurs through three distinct phases of membrane and cytoskeletal remodeling.
J Cell Biol. 2011 May 2; 193(3):455-64
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14 Jun 2011
Controversial, New Finding
DOI: 10.3410/f.11169956.12146054
This short investigative work demonstrates a surprising yet important finding that cadherin, a known cell-cell adhesion molecule, has a role in anchoring the actin cytoskeleton to the plasma membrane, independent of its role in cell-cell adhesion.
Using a single-cell wounding assay and live-cell imaging...Continue reading
Using a single-cell wounding assay and live-cell imaging...Continue reading
This short investigative work demonstrates a surprising yet important finding that cadherin, a known cell-cell adhesion molecule, has a role in anchoring the actin cytoskeleton to the plasma membrane, independent of its role in cell-cell adhesion.
Using a single-cell wounding assay and live-cell imaging techniques, the authors show that cadherins are recruited to the edge of single-cell wounds, overlapping with an actomyosin structure at the plasma membrane. In embryos with reduced cadherin, wound closure is retarded, which is accompanied by defective formation of the actomyosin ring necessary for healing. Interestingly, the authors show that cadherin localization to the wound edge is myosin II dependent. Future work to understand the role of myosin II at the initial stage of cadherin recruitment will help clarify the regulation and induction of wound repair.
Using a single-cell wounding assay and live-cell imaging techniques, the authors show that cadherins are recruited to the edge of single-cell wounds, overlapping with an actomyosin structure at the plasma membrane. In embryos with reduced cadherin, wound closure is retarded, which is accompanied by defective formation of the actomyosin ring necessary for healing. Interestingly, the authors show that cadherin localization to the wound edge is myosin II dependent. Future work to understand the role of myosin II at the initial stage of cadherin recruitment will help clarify the regulation and induction of wound repair.
Disclosures
None declared
Add Comment
Tang V: F1000Prime Recommendation of [Abreu-Blanco MT et al., J Cell Biol 2011, 193(3):455-64]. In F1000Prime, 14 Jun 2011; DOI: 10.3410/f.11169956.12146054. F1000Prime.com/11169956#eval12146054
16 Jun 2011
New Finding
DOI: 10.3410/f.11169956.12198055
This paper establishes a new model for cellular wound healing in Drosophila embryos, and yields the unexpected finding that DE-cadherin (the Drosophila ortholog of classical cadherin) is required for closure of wounds in single cells.
The authors used an elegant combination of laser wounding and 4-dimensional...Continue reading
The authors used an elegant combination of laser wounding and 4-dimensional...Continue reading
This paper establishes a new model for cellular wound healing in Drosophila embryos, and yields the unexpected finding that DE-cadherin (the Drosophila ortholog of classical cadherin) is required for closure of wounds in single cells.
The authors used an elegant combination of laser wounding and 4-dimensional (4D) microscopy to examine the response of early Drosophila embryos to damage. Confirming and extending findings from other models of single-cell wounding, wounds are closed by actomyosin-based motility. Interestingly, the cell adhesion molecule DE-cadherin is recruited to such single-cell wounds and is required in vivo for efficient wound repair. DE-cadherin may function to link the actin cytoskeleton to the plasma membrane compartment as the wounds close. These findings add a new player to our understanding of wound closure, and establish a promising new system for genetic studies of wound healing.
The authors used an elegant combination of laser wounding and 4-dimensional (4D) microscopy to examine the response of early Drosophila embryos to damage. Confirming and extending findings from other models of single-cell wounding, wounds are closed by actomyosin-based motility. Interestingly, the cell adhesion molecule DE-cadherin is recruited to such single-cell wounds and is required in vivo for efficient wound repair. DE-cadherin may function to link the actin cytoskeleton to the plasma membrane compartment as the wounds close. These findings add a new player to our understanding of wound closure, and establish a promising new system for genetic studies of wound healing.
Disclosures
None declared
Chisholm A: F1000Prime Recommendation of [Abreu-Blanco MT et al., J Cell Biol 2011, 193(3):455-64]. In F1000Prime, 16 Jun 2011; DOI: 10.3410/f.11169956.12198055. F1000Prime.com/11169956#eval12198055
07 Jul 2011
Confirmation, New Finding
DOI: 10.3410/f.11169956.12871068
This paper introduces the early Drosophila embryo as a novel model to study how cells heal their wounds. The authors establish that, in this system, single-cell wounds heal by a process that involves the assembly of actomyosin rings and membrane traffic. Strikingly, they report that DE-cadherin also accumulates...Continue reading
This paper introduces the early Drosophila embryo as a novel model to study how cells heal their wounds. The authors establish that, in this system, single-cell wounds heal by a process that involves the assembly of actomyosin rings and membrane traffic. Strikingly, they report that DE-cadherin also accumulates at the margins of wounds and is necessary for actomyosin rings and wound healing. This observation, thus, introduces a surprising, cell-autonomous role for this cell-cell adhesion molecule in a process independent of cell-cell interactions.
Wound healing takes two broad forms: the healing of multicellular wounds in tissues, and the healing of wounds of the plasma membrane within individual cells. The latter is a constant feature of day-to-day cellular homeostasis and occurs during disease, such as skin blistering disorders and muscular dystrophies. This paper introduces the early Drosophila embryo as a novel model system that brings powerful genetic tools to study single-cell wound healing. The authors analyse embryos before nuclear division or cytokinesis has occurred, thereby providing embryos that are effectively single cells that can be wounded by laser ablation. They demonstrate that wounds heal by the assembly of an actomyosin ring at the wound margin, which is also coupled to recruitment of vesicles to assist in sealing the membrane. These findings confirm earlier studies in Xenopus embryos and mammalian cells.
The striking finding of this report is the observation that DE-cadherin, a well-characterized cell-cell adhesion receptor, also accumulates with the actomyosin ring in newly-formed wound margins. Indeed, the actomyosin ring was shown to contribute to the localization of DE-cadherin, as cadherin failed to accumulate at wound margins when the actomyosin ring was perturbed by blocking Rho-kinase. Additionally, however, assembly of the actomyosin ring was perturbed, and wound healing delayed, when DE-cadherin was reduced in maternally-reduced DE-cadherin (shotgun) mutants. Together, these findings indicate that cadherin interacts cooperatively with cortical actomyosin to drive wound healing.
Further, as cadherin was recruited to, and appeared to functionally contribute to, the free margins of wounds, it suggests that, in this system, DE-cadherin may have been acting in an adhesion-independent manner (i.e. without requiring ligation of the cadherin extracellular domain). This is a very interesting implication of this paper that warrants further analysis of this and other systems. However, it should be noted that cadherin may be able to undergo ligation events even in single cells. Sabatini et al. {1} recently reported that N-cadherin on the surfaces of isolated cells participates in sealing macropinosomes, which derive from ruffling membranes. This required the cadherin ectodomain, implying that it might reflect cell-autonomous ligation of cadherin on closely-apposed ruffling membranes. Whether something similar occurs in single-cell wounds will be an interesting question for the future.
Wound healing takes two broad forms: the healing of multicellular wounds in tissues, and the healing of wounds of the plasma membrane within individual cells. The latter is a constant feature of day-to-day cellular homeostasis and occurs during disease, such as skin blistering disorders and muscular dystrophies. This paper introduces the early Drosophila embryo as a novel model system that brings powerful genetic tools to study single-cell wound healing. The authors analyse embryos before nuclear division or cytokinesis has occurred, thereby providing embryos that are effectively single cells that can be wounded by laser ablation. They demonstrate that wounds heal by the assembly of an actomyosin ring at the wound margin, which is also coupled to recruitment of vesicles to assist in sealing the membrane. These findings confirm earlier studies in Xenopus embryos and mammalian cells.
The striking finding of this report is the observation that DE-cadherin, a well-characterized cell-cell adhesion receptor, also accumulates with the actomyosin ring in newly-formed wound margins. Indeed, the actomyosin ring was shown to contribute to the localization of DE-cadherin, as cadherin failed to accumulate at wound margins when the actomyosin ring was perturbed by blocking Rho-kinase. Additionally, however, assembly of the actomyosin ring was perturbed, and wound healing delayed, when DE-cadherin was reduced in maternally-reduced DE-cadherin (shotgun) mutants. Together, these findings indicate that cadherin interacts cooperatively with cortical actomyosin to drive wound healing.
Further, as cadherin was recruited to, and appeared to functionally contribute to, the free margins of wounds, it suggests that, in this system, DE-cadherin may have been acting in an adhesion-independent manner (i.e. without requiring ligation of the cadherin extracellular domain). This is a very interesting implication of this paper that warrants further analysis of this and other systems. However, it should be noted that cadherin may be able to undergo ligation events even in single cells. Sabatini et al. {1} recently reported that N-cadherin on the surfaces of isolated cells participates in sealing macropinosomes, which derive from ruffling membranes. This required the cadherin ectodomain, implying that it might reflect cell-autonomous ligation of cadherin on closely-apposed ruffling membranes. Whether something similar occurs in single-cell wounds will be an interesting question for the future.
References
1.
Cadherins at cell-autonomous membrane contacts control macropinocytosis.
J Cell Sci 2011 Jun 15; Pt 12(124):2013-20
PMID: 21610088
Disclosures
None declared
Yap A: F1000Prime Recommendation of [Abreu-Blanco MT et al., J Cell Biol 2011, 193(3):455-64]. In F1000Prime, 07 Jul 2011; DOI: 10.3410/f.11169956.12871068. F1000Prime.com/11169956#eval12871068
F1000Prime Recommendations, Dissents and Comments for [Abreu-Blanco MT et al., J Cell Biol 2011, 193(3):455-64]. In F1000Prime, 23 May 2013; F1000Prime.com/11169956
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When single cells or tissues are injured, the wound must be repaired quickly in order to prevent cell death, loss of tissue integrity, and invasion by microorganisms. We describe Drosophila as a genetically tractable model to dissect the mechanisms of single-cell wound repair. By analyzing the expression and the effects of perturbations of actin, myosin, microtubules, E-cadherin, and the plasma membrane, we define three distinct phases in the repair process-expansion, contraction, and closure-and identify specific components required during each phase. Specifically, plasma membrane mobilization and assembly of a contractile actomyosin ring are required for this process. In addition, E-cadherin accumulates at the wound edge, and wound expansion is excessive in E-cadherin mutants, suggesting a role for E-cadherin in anchoring the actomyosin ring to the plasma membrane. Our results show that single-cell wound repair requires specific spatial and temporal cytoskeleton responses with distinct components and mechanisms required at different stages of the process.
PMID: 21518790
