Regulation of Hippo signaling by Jun kinase signaling during compensatory cell proliferation and regeneration, and in neoplastic tumors
Open accessAbstract
When cells undergo apoptosis, they can stimulate the proliferation of nearby cells, a process referred to as compensatory cell proliferation. The stimulation of proliferation in response to tissue damage or removal is also central to epimorphic regeneration. The Hippo signaling pathway has emerged as an important regulator of growth during normal development and oncogenesis from Drosophila to humans. Here we show that induction of apoptosis in the Drosophila wing imaginal disc stimulates activation of the Hippo pathway transcription factor Yorkie in surviving and nearby cells, and that Yorkie is required for the ability of the wing to regenerate after genetic ablation of the wing primordia. Induction of apoptosis activates Yorkie through the Jun kinase pathway, and direct activation of Jun kinase signaling also promotes Yorkie activation in the wing disc. We also show that depletion of neoplastic tumor suppressor genes, including lethal giant larvae and discs large, or activation of aPKC, activates Yorkie through Jun kinase signaling, and that Jun kinase activation is necessary, but not sufficient, for the disruption of apical-basal polarity associated with loss of lethal giant larvae. Our observations identify Jnk signaling as a modulator of Hippo pathway activity in wing imaginal discs, and implicate Yorkie activation in compensatory cell proliferation and disc regeneration.
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JNK signalling activity is converted from anti- to pro-tumour growth through downregulation of Hippo signalling, which ultimately leads to Yki activation.
“These findings are consistent with recent reports that JNK signalling activity is converted from anti- to pro-tumour growth through downregulation of Hippo signalling which ultimately leads to Yki activation (14,32).”
From A Tumour-Specific Molecular Network Promotes Tumour Growth in <i>Drosophila</i> by Enforcing a JNK-YKI Feedforward Loop (2023) · cites this paper as [14]
In “Regulation of Yki activity by neoplastic tumor suppressors” (page unavailable), the paper says Hippo signaling is inhibited by neoplastic tumor suppressor mutations, activating Yki, and that Yki activation is required for the resulting overgrowths. In “Regulation of Yki by Jnk signaling” (page unavailable), it identifies Jnk’s opposing apoptotic and proliferative roles but says how one outcome becomes favored—and how Jnk activates Yki—remains unknown. It therefore does not establish that downregulation of Hippo converts Jnk from anti- to pro-tumour activity. (LLM, conf=0.86)
Experimental — accuracy not yet measuredJNK and Yki are known to interact in a context-dependent manner.
“JNK and Yki are known to interact in a context-dependent manner (12-14,32), and increased JNK or Yki activity has been linked to tumour growth (12,33-35).”
From A Tumour-Specific Molecular Network Promotes Tumour Growth in <i>Drosophila</i> by Enforcing a JNK-YKI Feedforward Loop (2023) · cites this paper as [14]
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- Authors
- Sun, G., & Irvine, K. D.
- Affiliations
- Rutgers, The State University of New Jersey (US)
- Corresponding author
- Irvine, Kenneth D.
- Venue
- Developmental Biology
- Publisher
- Elsevier BV
- Published
- 2011-02
- Volume
- 350
- Issue
- 1
- Pages
- 139-151
- ISSN
- 0012-1606 (ISSN-L)
- PMC
- PMC3038240
- OpenAlex
- W2001202251
- Semantic Scholar
- 142209cb49895894705b4183b90076c5f3bfb5cb
- Cited by
- 219
- References
- 60
- Citations by year
- 2026: 2 · 2025: 6 · 2024: 8 · 2023: 6 · 2022: 7 · 2021: 9 · 2020: 17 · 2019: 15 · 2018: 15 · 2017: 14 · 2016: 20 · 2015: 23 · 2014: 21 · 2013: 22 · 2012: 14
- FWCI
- 7.83
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- www.elsevier.com/tdm/userlicense/1.0/ (tdm)
- www.elsevier.com/legal/tdmrep-license (tdm)
- www.elsevier.com/open-access/userlicense/1.0/ (vor, 897 d)
- doi.org/10.15223/policy-017 (stm-asf)
- doi.org/10.15223/policy-037 (stm-asf)
- doi.org/10.15223/policy-012 (stm-asf)
- doi.org/10.15223/policy-029 (stm-asf)
- doi.org/10.15223/policy-004 (stm-asf)
- Locations
- Developmental Biology (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- Howard Hughes Medical Institute
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Hippo pathway signaling and YAP/TAZ
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Developmental Biology and Gene Regulation
- Health Sciences › Medicine › Hepatology › Liver physiology and pathology
- Keywords
- Hippo signaling pathway, compensatory cell proliferation, epimorphic regeneration, wing imaginal disc, apoptosis, tumor suppressor, lethal giant larvae, Discs large, atypical protein kinase C, apical-basal polarity, Drosophila
- MeSH terms
- YAP-Signaling Proteins, Hippo Kinases, Animals, Drosophila melanogaster, Neoplasms, Nuclear Proteins, Regeneration, Wings, Animal, Signal Transduction, Trans-Activators, Genes, Tumor Suppressor, Apoptosis, Protein Serine-Threonine Kinases, Tumor Suppressor Proteins, Drosophila Proteins, Intracellular Signaling Peptides and Proteins, MAP Kinase Kinase 4, Cell Proliferation
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