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JNK signaling in Drosophila immunity and homeostasis
Ghada Tafesh-Edwards1, Ioannis Eleftherianos1
1Infection and Innate Immunity Lab, Department of Biological Sciences, Institute for Biomedical Sciences, The George Washington University, Science and Engineering Hall, 800 22nd Street NW, Washington DC, 20052, USA.
Abstract:
As members of the mitogen-activated protein kinase (MAPK) family, the c-Jun N-terminal kinases (JNKs) regulate cell responses to a wide range of extrinsic and intrinsic insults, including irradiation, reactive oxygen species (ROS), DNA damage, heat, bacterial antigens, and inflammatory cytokines. Particularly, JNK signaling regulates and promotes many important physiological processes that influence metabolic and tissue homeostasis, cell death/survival, and cell damage repair and ultimately impacts the lifespan of an organism. This diverse functionality causes a variety of tissue-specific and context-specific cellular responses, mediated by various cross talks between JNK and other cellular signaling pathways. Thus, highlighting its significance as a determinant of stress responses, JNK loss-of-function mutations have been implicated in a multitude of pathologies, including neurodegenerative diseases, diabetes, and cancer. Because JNK functions are specified in a context-dependent manner and can greatly vary, the underlying causes for these different outcomes remain largely unresolved despite the gained knowledge of many regulatory roles of JNK signaling during the past two decades. In Drosophila melanogaster, JNK signaling is conserved and required for immune responses, as well as the development for morphogenetic processes (embryonic dorsal closure and thorax closure). Therefore, Drosophila innate immunity provides the ideal model to understand the complex mechanisms underlying JNK activation and regulation. In the following, we review studies in Drosophila that highlight several mechanisms by which JNK signaling influences immunity and homeostasis.
Insights
The c-Jun N-terminal kinases (JNK) pathway regulates cellular stress responses and homeostasis. Studies in Drosophila reveal conserved JNK mechanisms crucial for immunity and development, offering insights into complex signaling.
Area of Science:
- Cellular Biology
- Molecular Biology
- Immunology
Background:
- Mitogen-activated protein kinase (MAPK) family members, c-Jun N-terminal kinases (JNKs), are critical regulators of cellular responses to diverse intrinsic and extrinsic stressors.
- JNK signaling influences vital physiological processes including metabolic homeostasis, cell death/survival, DNA repair, and organismal lifespan.
- Dysregulation of JNK signaling is implicated in pathologies such as neurodegenerative diseases, diabetes, and cancer, yet context-dependent mechanisms remain unclear.
Purpose of the Study:
- To review studies in Drosophila melanogaster that elucidate conserved mechanisms of JNK activation and regulation.
- To highlight how JNK signaling influences innate immunity and tissue homeostasis.
- To utilize Drosophila as a model system for understanding complex JNK pathway functions.
Main Methods:
- Review of existing literature focusing on JNK signaling in Drosophila.
- Analysis of conserved JNK pathway components and their roles in immunity and development.
- Examination of cross-talk between JNK and other signaling pathways in response to stress.
Main Results:
- JNK signaling is conserved in Drosophila and essential for embryonic development (dorsal and thorax closure) and innate immune responses.
- Drosophila provides an ideal model to dissect the complex regulatory networks governing JNK activation.
- Studies reveal specific mechanisms by which JNK influences immune function and maintains homeostasis.
Conclusions:
- JNK signaling plays a fundamental role in stress response, immunity, and homeostasis across species.
- Drosophila melanogaster serves as a powerful model for uncovering conserved JNK regulatory mechanisms.
- Further research in Drosophila can elucidate the context-dependent variations in JNK pathway outcomes relevant to human diseases.
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