Organogenesis and tumorigenesis: Insight from the JAK/STAT pathway in the <i>Drosophila</i> eye

Wang, Ying-Hsuan; Huang, Min-Lang

doi:10.1002/dvdy.22394

Cited by 33 publications

(26 citation statements)

References 132 publications

(244 reference statements)

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“…One possibility is that mutant germ cells respond as if they were male germ cells to the activating cytokine Unpaired secreted from the somatic gonadal cells. Although entirely speculative at this time, a role for sex-inappropriate activation of the Jak/Stat pathway in ovarian tumor formation is consistent with numerous studies that have connected hyperactive Jak/Stat signaling to other Drosophila tumor models,[44][45][46][47][48][49][50] and human cancers 51. …”

supporting

confidence: 68%

Sex, stem cells and tumors in the Drosophila ovary

Salz

2013

Fly

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The Drosophila Sex-lethal (Sxl) gene encodes a female-specific RNA binding protein that in somatic cells globally regulates all aspects of female-specific development and behavior. Sxl also has a critical, but less well understood, role in female germ cells. Germ cells without Sxl protein can adopt a stem cell fate when housed in a normal ovary, but fail to successfully execute the self-renewal differentiation fate switch. The failure to differentiate is accompanied by the inappropriate expression of a set of male specific markers, continued proliferation, and formation of a tumor. The findings in Chau et al., (2012) identify the germline stem cell maintenance factor nanos as one of its target genes, and suggest that Sxl enables the switch from germline stem cell to committed daughter cell by posttranscriptional downregulation of nanos expression. These studies provide the basis for a new model in which Sxl directly couples sexual identity with the self-renewal differentiation decision and raises several interesting questions about the genesis of the tumor phenotype.

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supporting

confidence: 68%

Sex, stem cells and tumors in the Drosophila ovary

Salz

2013

Fly

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“…Both Hippo and JAK/STAT pathways are involved in various aspects of tumorigenesis, such as tumor growth, EMT, and metastasis of tumor cells (Hou et al 2002;Pan 2010;Wang and Huang 2010;Harvey et al 2013). It will be interesting to study the interplay of these two pathways in cancer formation.…”

Section: Discussionmentioning

confidence: 99%

The Hippo Pathway Controls Border Cell Migration Through Distinct Mechanisms in Outer Border Cells and Polar Cells of the Drosophila Ovary

Lin¹,

Yeh²,

Wang

et al. 2014

Genetics

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The Hippo pathway is a key signaling cascade in controlling organ size. The core components of this pathway are two kinases, Hippo (Hpo) and Warts (Wts), and a transcriptional coactivator, Yorkie (Yki). Yes-associated protein (YAP, a Yki homolog in mammals) promotes epithelial-mesenchymal transition and cell migration in vitro. Here, we use border cells in the Drosophila ovary as a model to study Hippo pathway functions in cell migration in vivo. During oogenesis, polar cells secrete Unpaired (Upd), which activates JAK/STAT signaling of neighboring cells and specifies them into outer border cells. The outer border cells form a cluster with polar cells and undergo migration. We find that hpo and wts are required for migration of the border cell cluster. In outer border cells, overexpression of hpo disrupts polarization of the actin cytoskeleton and attenuates migration. In polar cells, knockdown of hpo and wts or overexpression of yki impairs border cell induction and disrupts migration. These manipulations in polar cells reduce JAK/STAT activity in outer border cells. Expression of upd-lacZ is increased and decreased in yki and hpo mutant polar cells, respectively. Furthermore, forced expression of upd in polar cells rescues defects of border cell induction and migration caused by wts knockdown. These results suggest that Yki negatively regulates border cell induction by inhibiting JAK/STAT signaling. Together, our data elucidate two distinct mechanisms of the Hippo pathway in controlling border cell migration: (1) in outer border cells, it regulates polarized distribution of the actin cytoskeleton; (2) in polar cells, it regulates upd expression to control border cell induction and migration.

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“…Indeed, the aberrant activation of JAK/STAT signaling has also been implicated in a variety of malignant tumors in Drosophila as well as in mammals (48)(49)(50). In imaginal discs, the tumorous overgrowths by mutations of Polycomb group (PcG) genes or inter-or intracellular cooperation of oncogenic Ras V12 and scrib − mutations resulted in abnormal activation of JAK/STAT signaling (51,52).…”

Section: Upd Activates Jak/stat Signaling In Early Regenerating Discs Tomentioning

confidence: 99%

During Drosophila disc regeneration, JAK/STAT coordinates cell proliferation with Dilp8-mediated developmental delay

Katsuyama

Comoglio

Seimiya

et al. 2015

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

108

150

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Regeneration of fragmented Drosophila imaginal discs occurs in an epimorphic manner involving local cell proliferation at the wound site. After disc fragmentation, cells at the wound site activate a restoration program through wound healing, regenerative cell proliferation, and repatterning of the tissue. However, the interplay of signaling cascades driving these early reprogramming steps is not well-understood. Here, we profiled the transcriptome of regenerating cells in the early phase within 24 h after wounding. We found that JAK/STAT signaling becomes activated at the wound site and promotes regenerative cell proliferation in cooperation with Wingless (Wg) signaling. In addition, we showed that the expression of Drosophila insulin-like peptide 8 (dilp8), which encodes a paracrine peptide to delay the onset of pupariation, is controlled by JAK/STAT signaling in early regenerating discs. Our findings suggest that JAK/STAT signaling plays a pivotal role in coordinating regenerative disc growth with organismal developmental timing.

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Organogenesis and tumorigenesis: Insight from the JAK/STAT pathway in the Drosophila eye

Cited by 33 publications

References 132 publications

Sex, stem cells and tumors in the Drosophila ovary

Sex, stem cells and tumors in the Drosophila ovary

The Hippo Pathway Controls Border Cell Migration Through Distinct Mechanisms in Outer Border Cells and Polar Cells of the Drosophila Ovary

During Drosophila disc regeneration, JAK/STAT coordinates cell proliferation with Dilp8-mediated developmental delay

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