Oxidative Stress Orchestrates Cell Polarity to Promote Embryonic Wound Healing

Hunter, Miranda V.; Willoughby, Patrick Morley; Bruce, Ashley E.E.; Fernández-González, Rodrigo

doi:10.1016/j.devcel.2018.10.013

Cited by 59 publications

(73 citation statements)

References 61 publications

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“…Intracellular ROS Contributes to the Activation of Macrophages An increase in TCFB probe fluorescence was observed within hemocytes that were close to the wound site (Figures 2A and 2A 0 ). It has previously been demonstrated that ROS levels increase in the epithelia around a wound in both Drosophila and zebrafish embryos (Hunter et al, 2018). Appropriate levels of ROS in tissues are maintained by a series of enzymes, including superoxide dismutase (Sod) and catalase (Nordberg and Arné r, 2001).…”

Section: Injury-induced Ros Burst Is Essential For Upd-3 Expressionmentioning

confidence: 99%

“…The migration of embryonic hemocytes to sites of damage where H 2 O 2 is produced is regulated by the apoptotic receptor Draper (drpr), together with the Src family kinase Src42A and a Syk homolog, Shark ( Figure S4A) (Evans et al, 2015). H 2 O 2 drives wound closure through Src42A, which promotes polarization of junctions and cytoskeleton around wounds (Hunter et al, 2018). A previous study demonstrated that homozygous drpr D5 adults have reduced longevity (Draper et al, 2014).…”

Section: Induction Of Upd-3 Is Dependent On the Src42a/shark/ Draper mentioning

confidence: 99%

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Intramacrophage ROS Primes the Innate Immune System via JAK/STAT and Toll Activation

Chakrabarti

Visweswariah

2020

Cell Reports

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Section: Injury-induced Ros Burst Is Essential For Upd-3 Expressionmentioning

confidence: 99%

Section: Induction Of Upd-3 Is Dependent On the Src42a/shark/ Draper mentioning

confidence: 99%

Intramacrophage ROS Primes the Innate Immune System via JAK/STAT and Toll Activation

Chakrabarti

Visweswariah

2020

Cell Reports

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“…In particular, Ca 2+ diminished ROS from ROS generation sites within the mitochondria under normal conditions and enhanced ROS generation when generation sites were inhibited by pharmacological agents . Further, quantitative in vivo microscopy in Drosophila and zebrafish embryos identified ROS as crucial signals that regulate cell polarity after wounding . Hunter et al utilized fluorescent imaging after wounding Drosophila embryos and demonstrated Ca 2+ ‐dependent mitochondrial ROS production correlates with the site of actomyosin cable assembly.…”

Section: Feedback From Physiological Signaling Ensures Robustness Of mentioning

confidence: 99%

“…103 Further, quantitative in vivo microscopy in Drosophila and zebrafish embryos identified ROS as crucial signals that regulate cell polarity after wounding. 104 Hunter et al utilized fluorescent imaging after wounding Drosophila embryos and demonstrated Ca 2+ -dependent mitochondrial ROS production correlates with the site of actomyosin cable assembly. This suggests that wound-induced ROS production promotes healing in Drosophila and zebrafish embryos.…”

Section: Feedback From Physiological Signaling Ensures Robustness Omentioning

confidence: 99%

Interplay between morphogen‐directed positional information systems and physiological signaling

Huizar

Soundarrajan

Paravitorghabeh

et al. 2019

Developmental Dynamics

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The development of an organism from an undifferentiated single cell into a spatially complex structure requires spatial patterning of cell fates across tissues. Positional information, proposed by Lewis Wolpert in 1969, has led to the characterization of many components involved in regulating morphogen signaling activity. However, how morphogen gradients are established, maintained, and interpreted by cells still is not fully understood. Quantitative and systems‐based approaches are increasingly needed to define general biological design rules that govern positional information systems in developing organisms. This short review highlights a selective set of studies that have investigated the roles of physiological signaling in modulating and mediating morphogen‐based pattern formation. Similarities between neural transmission and morphogen‐based pattern formation mechanisms suggest underlying shared principles of active cell‐based communication. Within larger tissues, neural networks provide directed information, via physiological signaling, that supplements positional information through diffusion. Further, mounting evidence demonstrates that physiological signaling plays a role in ensuring robustness of morphogen‐based signaling. We conclude by highlighting several outstanding questions regarding the role of physiological signaling in morphogen‐based pattern formation. Elucidating how physiological signaling impacts positional information is critical for understanding the close coupling of developmental and cellular processes in the context of development, disease, and regeneration.

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“…Recent studies have addressed the role of mitochondria in tissue repair, showing that mitochondrial reactive oxygen species (ROS) promote wound healing by regulating F-actin and Myosin at the wound edge, either by acting on Rho GTPases (Muliyil and Narasimha, 2014; Xu and Chisholm, 2014) or on cell-cell junction remodeling (Hunter et al, 2018). In this work, we show that the mitochondrial dynamics machinery is required for repair, as mutants for these proteins fail to close epithelial wounds.…”

Section: Introductionmentioning

confidence: 99%

Drp1-mediated mitochondrial fission regulates calcium and F-actin dynamics during wound healing

Ponte

Carvalho

Gagliardi

et al. 2019

Preprint

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Mitochondria adapt to cellular needs by changes in morphology through fusion and fission events, referred to as mitochondrial dynamics. Mitochondrial function and morphology are intimately connected and the dysregulation of mitochondrial dynamics is linked to several human diseases. In this work, we investigated the role of mitochondrial dynamics in wound healing in the Drosophila embryonic epidermis. Mutants for mitochondrial fusion and fission proteins fail to close their wounds, indicating that the regulation of mitochondrial dynamics is required for wound healing. By live-imaging, we found that loss of function of the mitochondrial fission protein Dynamin-related protein 1 (Drp1) compromises the increase of cytosolic and mitochondrial calcium upon wounding and leads to F-actin defects at the wound edge, culminating in wound healing impairment. Our results highlight a new role for mitochondrial dynamics in the regulation of calcium and F-actin during epithelial repair.SummaryWe show that mitochondrial dynamics proteins are required for epithelial repair. In particular, Drp1 loss-of-function leads to defects in the dynamics of cytosolic and mitochondrial calcium and F-actin upon wounding.

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Oxidative Stress Orchestrates Cell Polarity to Promote Embryonic Wound Healing

Abstract: Graphical AbstractHighlights d Wound-induced ROS production promotes healing in Drosophila and zebrafish embryos d ROS direct redistribution of junctions and the cytoskeleton at the wound margin d Src oxidation contributes to E-cadherin and myosin polarization around wounds

Cited by 59 publications

References 61 publications

Intramacrophage ROS Primes the Innate Immune System via JAK/STAT and Toll Activation

Intramacrophage ROS Primes the Innate Immune System via JAK/STAT and Toll Activation

Interplay between morphogen‐directed positional information systems and physiological signaling

Drp1-mediated mitochondrial fission regulates calcium and F-actin dynamics during wound healing

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