Abstract

The Jun N-terminal kinase (JNK) pathway is an evolutionary conserved kinase cascade best known for its roles during stress-induced apoptosis and tumor progression. Recent findings, however, have identified new roles for this pleiotropic pathway in stem cells during regenerative responses and in cellular plasticity. Here, we provide an overview of recent findings about the new roles of JNK signaling in stem cell biology using two well-established Drosophila models: the testis and the intestine. We highlight the pathway’s roles in processes such as proliferation, death, self-renewal and reprogramming, and discuss the known parallels between flies and mammals.

Highlights

  • Stem cells are essential for the maintenance of many adult tissues, and they support tissues as a result of two key properties: (1) their capacity for self-renewal, by which they can proliferate while maintaining their stemness, and (2) their ability to produce differentiating daughter cells, which replace effete cells in tissues with a high cellular turnover

  • We focus on Jun N-terminal kinase (JNK) function in two well-studied Drosophila stem cell models, the testis and the intestine, describing recent advances and relating these discoveries to relevant mammalian counterparts

  • IL-6 secretion, but to symmetric division. This involves in this cell type IL-6 expression is controlled by the Hh pathway downstream of JNK acchanging the orientation of intestinal stem cells (ISCs) mitotic spindle relative to the plane of the epithelium from tivation [64]

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Summary

Introduction

Stem cells are essential for the maintenance of many adult tissues, and they support tissues as a result of two key properties: (1) their capacity for self-renewal, by which they can proliferate while maintaining their stemness, and (2) their ability to produce differentiating daughter cells, which replace effete cells in tissues with a high cellular turnover. Bsk/JNK phosphorylates AP-1 components Jun and Fos, which are represented by orthologs in Drosophila, Jun-related antigen (Jra) and Kayak (Kay), respectively, as (Wgn) and Grindelwald (Grnd) appears to activate JNK upregulates exclusively, while other [4]. JNK signaling can be activated intrinsically, for example, through the redox-sensitive MAPKKK Apoptotic signal-regulating kinase 1 (Ask1) [12] Extrinsic signals such as the Egr/TNFα ligand Egr/TNFα can bind the TNFα receptors(TNFRs). The STRIPAK complex that binds to Hep/JNKK, Bsk/JNK and AP-1 a inhibits the pathway. In both Drosophila and higher organisms, JNK has pleiotropic effects, including apoptosis, proliferation, differentiation, cell migration, tumorigenesis, and cell competition (reviewed in [1,6,13]). We focus on JNK function in two well-studied Drosophila stem cell models, the testis and the intestine, describing recent advances and relating these discoveries to relevant mammalian counterparts

The Role of JNK in the Drosophila Testis during Homeostasis
The Role of JNK in the Drosophila Testis during Stress
The Roles of JNK in Recovery from Stress and in Germline Plasticity
Making Sense of JNK Versatility in Drosophila and Vertebrate Testes
JNK Signaling in Stress Responses and Aging in the Drosophila Intestine
Concluding Remarks
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