Regulating cell morphogenesis: The drosophila jun N‐terminal kinase pathway

Ríos-Barrera, Luis Daniel; Riesgo-Escovar, Juan R.

doi:10.1002/dvg.22354

Cited by 68 publications

(68 citation statements)

References 147 publications

(266 reference statements)

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“…56, 57 Selective activation of subsets of these upstream factors directs whether JNK activity is pro-apoptotic or pro-survival. 58 How activation of the same JNK (flies only have one JNK homolog) by distinct upstream factors can trigger different outcomes as diverse as death or survival remains largely enigmatic.…”

Section: The Many Mechanisms Of Caspase-driven Aipmentioning

confidence: 99%

Killers creating new life: caspases drive apoptosis-induced proliferation in tissue repair and disease

2017

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Apoptosis is a carefully orchestrated and tightly controlled form of cell death, conserved across metazoans. As the executioners of apoptotic cell death, cysteine-dependent aspartate-directed proteases (caspases) are critical drivers of this cellular disassembly. Early studies of genetically programmed cell death demonstrated that the selective activation of caspases induces apoptosis and the precise elimination of excess cells, thereby sculpting structures and refining tissues. However, over the past decade there has been a fundamental shift in our understanding of the roles of caspases during cell death—a shift precipitated by the revelation that apoptotic cells actively engage with their surrounding environment throughout the death process, and caspases can trigger a myriad of signals, some of which drive concurrent cell proliferation regenerating damaged structures and building up lost tissues. This caspase-driven compensatory proliferation is referred to as apoptosis-induced proliferation (AiP). Diverse mechanisms of AiP have been found across species, ranging from planaria to mammals. In this review, we summarize the current knowledge of AiP and we highlight recent advances in the field including the involvement of reactive oxygen species and macrophage-like immune cells in one form of AiP, novel regulatory mechanisms affecting caspases during AiP, and emerging clinical data demonstrating the critical importance of AiP in cancer.

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Section: The Many Mechanisms Of Caspase-driven Aipmentioning

confidence: 99%

Killers creating new life: caspases drive apoptosis-induced proliferation in tissue repair and disease

2017

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“…In many contexts, JNK signaling leads to apoptosis, perhaps a remnant of this pathway’s ancestral function in stress response (Ríos-Barrera and Riesgo-Escovar, 2013). JNK signaling may have started to regulate cytoskeletal functions in multicellular organisms to facilitate delamination or extrusion of defective cells.…”

Section: Resultsmentioning

confidence: 99%

“…JNK can exert its proapoptotic effect through phosphorylation of Jun, a component of the AP-1 transcriptional activator, or of other cellular proteins (Bogoyevitch and Kobe, 2006). It is important to note, however, that JNK signaling does not always trigger apoptosis (Weston and Davis, 2007) and has been shown to control nonapoptotic processes such as cytoskeletal rearrangements (Homsy et al., 2006), cell migration (Ríos-Barrera and Riesgo-Escovar, 2013), and cell proliferation (Shaulian and Karin, 2002) during development and regeneration. It is generally thought that the cellular context or the activity of other signaling pathways determines whether JNK signaling leads to apoptosis or not.…”

Section: Introductionmentioning

confidence: 99%

The Dpp/TGFβ-Dependent Corepressor Schnurri Protects Epithelial Cells from JNK-Induced Apoptosis in Drosophila Embryos

et al. 2014

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SummaryJun N-terminal kinase (JNK) often mediates apoptosis in response to cellular stress. However, during normal development, JNK signaling controls a variety of live cell behaviors, such as during dorsal closure in Drosophila embryos. During this process, the latent proapoptotic activity of JNK becomes apparent following Dpp signaling suppression, which leads to JNK-dependent transcriptional activation of the proapoptotic gene reaper. Dpp signaling also protects cells from JNK-dependent apoptosis caused by epithelial disruption. We find that repression of reaper transcription by Dpp is mediated by Schnurri. Moreover, reporter gene analysis shows that a transcriptional regulatory module comprising AP-1 and Schnurri binding sites located upstream of reaper integrate the activities of JNK and Dpp. This arrangement allows JNK to control a migratory behavior without triggering apoptosis. Dpp plays a dual role during dorsal closure. It cooperates with JNK in stimulating cell migration and also prevents JNK from inducing apoptosis.

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“…In mammals, JNK regulates cell adhesion through effects on b-catenin and adherens junctions (Lee et al 2009(Lee et al , 2011You et al 2013). Cell adhesion effects are also associated with JNK in Drosophila, such as its role in dorsal closure and wound healing (Bosch et al 2005;Rios-Barrera and Riesgo-Escovar 2013). Correct cell-cell contact and cell polarization may be required for appropriate processing and secretion or other transport of Dpp from the peripodial epithelium.…”

Section: Discussionmentioning

confidence: 99%

Dual Role of Jun N-Terminal Kinase Activity in Bone Morphogenetic Protein-Mediated Drosophila Ventral Head Development

2015

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The Drosophila bone morphogenetic protein encoded by decapentaplegic (dpp) controls ventral head morphogenesis by expression in the head primordia, eye-antennal imaginal discs. These are epithelial sacs made of two layers: columnar disc proper cells and squamous cells of the peripodial epithelium. dpp expression related to head formation occurs in the peripodial epithelium; cisregulatory mutations disrupting this expression display defects in sensory vibrissae, rostral membrane, gena, and maxillary palps. Here we document that disruption of this dpp expression causes apoptosis in peripodial cells and underlying disc proper cells. We further show that peripodial Dpp acts directly on the disc proper, indicating that Dpp must cross the disc lumen to act. We demonstrate that palp defects are mechanistically separable from the other mutant phenotypes; both are affected by the c-Jun N-terminal kinase pathway but in opposite ways. Slight reduction of both Jun N-terminal kinase and Dpp activity in peripodial cells causes stronger vibrissae, rostral membrane, and gena defects than Dpp alone; additionally, strong reduction of Jun N-terminal kinase activity alone causes identical defects. A more severe reduction of dpp results in similar vibrissae, rostral membrane, and gena defects, but also causes mutant maxillary palps. This latter defect is correlated with increased peripodial Jun N-terminal kinase activity and can be caused solely by ectopic activation of Jun N-terminal kinase. We conclude that formation of sensory vibrissae, rostral membrane, and gena tissue in head morphogenesis requires the action of Jun N-terminal kinase in peripodial cells, while excessive Jun N-terminal kinase signaling in these same cells inhibits the formation of maxillary palps.KEYWORDS bone morphogenetic protein (BMP); decapentaplegic (dpp); Jun N-terminal kinase (JNK); apoptosis; head morphogenesis; Drosophila B ONE morphogenetic proteins (BMPs) are critical participants in patterning, growth control, and morphogenesis during animal development. They are processed, secreted proteins that signal by binding to transmembrane serine-threonine kinases. Many of the component proteins involved in regulating receipt and transmission of the BMP signal have been elucidated (Ramel and Hill 2012). However, how BMPs disperse from their sources to the cells bearing their receptors remains an active area of study.The major Drosophila BMP, decapentaplegic (dpp), is employed repeatedly during embryonic and larval fly development for both short-range (Panganiban et al. 1990;Chen et al. 2011) and long-range (Entchev et al. 2000;Teleman and Cohen 2000;Shimmi et al. 2005) signaling. dpp is required for the correct formation of all adult epidermal structures derived from imaginal discs. These are epithelial saclike structures that contain a columnar epithelium called the disc proper (DP) and a squamous epithelium called the peripodial membrane or peripodial epithelium (PE), separated by a lumen. The eye and adult head capsule, including sensory structur...

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Regulating cell morphogenesis: The drosophila jun N‐terminal kinase pathway

Cited by 68 publications

References 147 publications

Killers creating new life: caspases drive apoptosis-induced proliferation in tissue repair and disease

Killers creating new life: caspases drive apoptosis-induced proliferation in tissue repair and disease

The Dpp/TGFβ-Dependent Corepressor Schnurri Protects Epithelial Cells from JNK-Induced Apoptosis in Drosophila Embryos

Dual Role of Jun N-Terminal Kinase Activity in Bone Morphogenetic Protein-Mediated Drosophila Ventral Head Development

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