<i>cdc37</i> is essential for JNK pathway activation and wound closure in <i>Drosophila</i>

Lee, Chan Wool; Kwon, Yumi; Lee, Youngbin; Park, Min Yoon; Choe, Kwang Min

doi:10.1091/mbc.e18-12-0822

Cited by 10 publications

(7 citation statements)

References 48 publications

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“…Next, we disrupted JNK signalling, which is known to be key in developmental morphogenetic episodes such as dorsal closure (Tafesh-Edwards & Eleftherianos, 2020), and in wound healing, both in the formation of actomyosin cables and for associated cell shape changes (Kwon et al, 2010; Lee et al, 2019).…”

Section: Resultsmentioning

confidence: 99%

AI reveals a damage signalling hierarchy that coordinates different cell behaviours driving wound re-epithelialisation

Turley,

Robertson,

Chenchiah

et al. 2024

Preprint

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One of the key tissue movements driving closure of a wound is re-epithelialisation. Earlier wound healing studies have described the dynamic cell behaviours that contribute to wound re-epithelialisation, including cell division, cell shape changes and cell migration, as well as the signals that might regulate these cell behaviours. Here, we use a series of deep learning tools to quantify the contributions of each of these cell behaviours from movies of repairing wounds in theDrosophilapupal wing epithelium. We test how each is altered following knockdown of the conserved wound repair signals, Ca2+and JNK, as well as ablation of macrophages which supply growth factor signals believed to orchestrate aspects of the repair process. Our genetic perturbation experiments provide quantifiable insights regarding how these wound signals impact cell behaviours. We find that Ca2+signalling is a master regulator required for all contributing cell behaviours; JNK signalling primarily drives cell shape changes and divisions, whereas signals from macrophages regulate largely cell migration and proliferation. Our studies show AI to be a valuable tool for unravelling complex signalling hierarchies underlying tissue repair.

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Section: Resultsmentioning

confidence: 99%

AI reveals a damage signalling hierarchy that coordinates different cell behaviours driving wound re-epithelialisation

Turley,

Robertson,

Chenchiah

et al. 2024

Preprint

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“…Similar to mammals, ubiquitination of TAK1 terminates JNK signaling in the innate immune response. Cdc37 also acts as a molecular chaperone for TAK1 in Drosophila, as knockdown of Cdc37 in larvae induces a decrease in TAK1 protein abundance (Lee et al, 2019).…”

Section: B the P38 And C-jun N-terminal Kinase Signaling Pathwaysmentioning

confidence: 99%

Regulation of Mitogen-Activated Protein Kinase Signaling Pathways by the Ubiquitin-Proteasome System and Its Pharmacological Potential

2021

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“…Following injury, larval barrier epithelial cells at the wound edge locally detach from the apical cuticle and migrate into the wound gap. This process requires both JNK signaling ( Galko and Krasnow 2004 ; Lesch et al 2010 ; Lee et al 2019 ) and Pvr signaling ( Wu et al 2009 ). The latter is required in some manner for epithelial extension into the wound site, though it has been difficult to identify downstream genes of this pathway given a lack of pathway reporters that function well in vivo during the larval stage.…”

Section: Introductionmentioning

confidence: 99%

Pvr and distinct downstream signaling factors are required for hemocyte spreading and epidermal wound closure at Drosophila larval wound sites

Tsai

Wang

Jacobson

et al. 2021

G3 Genes|Genomes|Genetics

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Tissue injury is typically accompanied by inflammation. In Drosophila melanogaster larvae, wound-induced inflammation involves adhesive capture of hemocytes at the wound surface followed by hemocyte spreading to assume a flat, lamellar morphology. The factors that mediate this cell spreading at the wound site are not known. Here, we discover a role for the platelet-derived growth factor/vascular endothelial growth factor-related receptor (Pvr) and its ligand, Pvf1, in blood cell spreading at the wound site. Pvr and Pvf1 are required for spreading in vivo and in an in vitro spreading assay where spreading can be directly induced by Pvf1 application or by constitutive Pvr activation. In an effort to identify factors that act downstream of Pvr, we performed a genetic screen in which select candidates were tested to determine if they could suppress the lethality of Pvr overexpression in the larval epidermis. Some of the suppressors identified are required for epidermal wound closure (WC), another Pvr-mediated wound response, some are required for hemocyte spreading in vitro, and some are required for both. One of the downstream factors, Mask, is also required for efficient wound-induced hemocyte spreading in vivo. Our data reveal that Pvr signaling is required for wound responses in hemocytes (cell spreading) and defines distinct downstream signaling factors that are required for either epidermal WC or hemocyte spreading.

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cdc37 is essential for JNK pathway activation and wound closure in Drosophila

Cited by 10 publications

References 48 publications

AI reveals a damage signalling hierarchy that coordinates different cell behaviours driving wound re-epithelialisation

AI reveals a damage signalling hierarchy that coordinates different cell behaviours driving wound re-epithelialisation

Regulation of Mitogen-Activated Protein Kinase Signaling Pathways by the Ubiquitin-Proteasome System and Its Pharmacological Potential

Pvr and distinct downstream signaling factors are required for hemocyte spreading and epidermal wound closure at Drosophila larval wound sites

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