Transcriptional regulation of Profilin during wound closure in <i>Drosophila</i> larvae

Brock, Amanda R.; Wang, Yan; Berger, Susanne; Renkawitz‐Pohl, Renate; Han, Violet C.; Wu, Yujane; Galko, Michael J.

doi:10.1242/jcs.107490

Cited by 45 publications

(52 citation statements)

References 61 publications

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“…cytoskeletal regulators, such as Profilin (Brock et al, 2012). However, we find that phosphorylated ERK does not appear to exert its effect on embryonic wound healing through transcription, because inhibiting transcription does not affect the rate of healing.…”

Section: Discussionmentioning

confidence: 61%

ERK and phosphoinositide 3-kinase temporally coordinate different modes of actin-based motility during embryonic wound healing

Li¹,

Zhang²,

Soto³

et al. 2013

Development

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SummaryEmbryonic wound healing provides a perfect example of efficient recovery of tissue integrity and homeostasis, which is vital for survival. Tissue movement in embryonic wound healing requires two functionally distinct actin structures: a contractile actomyosin cable and actin protrusions at the leading edge. Here, we report that the discrete formation and function of these two structures is achieved by the temporal segregation of two intracellular upstream signals and distinct downstream targets. The sequential activation of ERK and phosphoinositide 3-kinase (PI3K) signalling divides Xenopus embryonic wound healing into two phases. In the first phase, activated ERK suppresses PI3K activity, and is responsible for the activation of Rho and myosin-2, which drives actomyosin cable formation and constriction. The second phase is dominated by restored PI3K signalling, which enhances Rac and Cdc42 activity, leading to the formation of actin protrusions that drive migration and zippering. These findings reveal a new mechanism for coordinating different modes of actin-based motility in a complex tissue setting, namely embryonic wound healing.

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Section: Discussionmentioning

confidence: 61%

ERK and phosphoinositide 3-kinase temporally coordinate different modes of actin-based motility during embryonic wound healing

Li¹,

Zhang²,

Soto³

et al. 2013

Development

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“…AP-1 sequence motifs are also required for woundinduced gene expression of Ddc and ple, although it is still unclear in Drosophila embryos whether the JNK pathway acts upstream of the AP-1 (Jun/Fos DNA binding) sites in this context (11,12). There are many other epidermal wound-induced genes for which the JNK pathway is unquestionably crucial (6,7,9,10,36). It seems logical that many overlapping signaling pathways generate the specificity to regulate wound-induced genes, because it would be catastrophic to activate the entire suite of wound repair genes whenever the individual pathways involving ERK, JNK, or Toll are activated (Fig.…”

Section: Discussionmentioning

confidence: 99%

Toll pathway is required for wound-induced expression of barrier repair genes in the Drosophila epidermis

Capilla

Karachentsev

Patterson

et al. 2017

Proc. Natl. Acad. Sci. U.S.A.

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The epidermis serves as a protective barrier in animals. After epidermal injury, barrier repair requires activation of many wound response genes in epidermal cells surrounding wound sites. Two such genes in Drosophila encode the enzymes dopa decarboxylase (Ddc) and tyrosine hydroxylase (ple). In this paper we explore the involvement of the Toll/NF-κB pathway in the localized activation of wound repair genes around epidermal breaks. Robust activation of wound-induced transcription from ple and Ddc requires Toll pathway components ranging from the extracellular ligand Spätzle to the Dif transcription factor. Epistasis experiments indicate a requirement for Spätzle ligand downstream of hydrogen peroxide and protease function, both of which are known activators of wound-induced transcription. The localized activation of Toll a few cell diameters from wound edges is reminiscent of local activation of Toll in early embryonic ventral hypoderm, consistent with the hypothesis that the dorsal–ventral patterning function of Toll arose from the evolutionary cooption of a morphogen-responsive function in wound repair. Furthermore, the combinatorial activity of Toll and other signaling pathways in activating epidermal barrier repair genes can help explain why developmental activation of the Toll, ERK, or JNK pathways alone fail to activate wound repair loci.

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“…For example, Pvf1 null mutants are adult viable, but mutant males show morphological defects of the external genitalia (Macias et al, 2004), a phenotype seen in slpr BS06 zygotic mutant males, in which JNK signaling is impaired (Polaski et al, 2006). Pvf1/Pvr and JNK signaling are also required for wound healing, regulating distinct aspects of the process (Brock et al, 2012;Wu et al, 2009).…”

Section: Synthetic Lethal Interaction Between the Jnk Pathway And Pvf1mentioning

confidence: 99%

Pvr receptor tyrosine kinase promotes tissue closure by coordinating corpse removal and epidermal zippering

et al. 2015

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A leading cause of human birth defects is the incomplete fusion of tissues, often manifested in the palate, heart, or neural tube. To investigate the molecular control of tissue fusion, embryonic dorsal closure and pupal thorax closure in Drosophila are useful experimental models. We find that Pvr mutants have defects in dorsal midline closure with incomplete amnioserosa internalization and epidermal zippering, as well as cardia bifida. These defects are relatively mild in comparison to those seen with other signaling mutants such as the JNK pathway, and we demonstrate that JNK signaling is not perturbed by altering Pvr receptor tyrosine kinase activity. Rather, modulation of Pvr levels in the ectoderm has an impact on PIP3 membrane accumulation consistent with a link to PI3K signal transduction. Polarized PI3K activity influences protrusive activity from the epidermal leading edge and protrusion area changes in accord with Pvr signaling intensity, providing a possible mechanism to explain Pvr mutant phenotypes. Tissue specific rescue experiments indicate a partial requirement in epithelial tissue, but confirm the essential role of Pvr in the hemocytes for embryonic survival. Taken together, we argue that inefficient removal of the internalizing amnioserosa tissue by mutant hemocytes coupled with impaired midline zippering of mutant epithelium creates a situation in some embryos where dorsal midline closure is incomplete. Based on these observations, we suggest that efferocytosis (corpse clearance) could contribute to proper tissue closure and thus may underlie some congenital birth defects.

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Transcriptional regulation of Profilin during wound closure in Drosophila larvae

Cited by 45 publications

References 61 publications

ERK and phosphoinositide 3-kinase temporally coordinate different modes of actin-based motility during embryonic wound healing

ERK and phosphoinositide 3-kinase temporally coordinate different modes of actin-based motility during embryonic wound healing

Toll pathway is required for wound-induced expression of barrier repair genes in the Drosophila epidermis

Pvr receptor tyrosine kinase promotes tissue closure by coordinating corpse removal and epidermal zippering

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