Localized JAK/STAT signaling is required for oriented cell rearrangement in a tubular epithelium

Johansen, Katherine A.; Iwaki, D.David; Lengyel, Judith A.

doi:10.1242/dev.00202

Cited by 68 publications

(67 citation statements)

References 62 publications

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“…Furthermore, expression of an activated form of HOP in a large number of anterior follicle cells led to a dramatic increase in the level of accumulation of STAT protein in those cells. This observed increase in STAT protein in response to excess JAK activity is consistent with previous studies that showed that STAT protein levels are dramatically reduced, when compared with wild type, in upd, hop and dome (also called mom) mutant embryos (Chen et al, 2002), and are upregulated upon overexpression of UPD and HOP TUM (Johansen et al, 2003). Thus, both the subcellular localization and the overall level of STAT protein respond to the level of activity of the pathway.…”

Section: Requirement For Continuous Stat Activity Throughout Border Csupporting

confidence: 90%

Requirement for JAK/STAT signaling throughout border cell migration inDrosophila

2005

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detectable change in the expression of cell fate markers. At later times, cell fate changes became evident, indicating that border cell fate is labile. JAK/STAT signaling was also required for organization of the border cell cluster. Finally, we show that both the accumulation of STAT protein and nuclear accumulation are positively regulated by JAK/STAT activity. The activity of the pathway is negatively regulated by overexpression of a SOCS protein and by blocking endocytosis. Together, our findings suggest that the requirement for STAT in border cells extends beyond the initial specification and delamination of cells from the epithelium.

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Section: Requirement For Continuous Stat Activity Throughout Border Csupporting

confidence: 90%

Requirement for JAK/STAT signaling throughout border cell migration inDrosophila

2005

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“…For UAS/GAL4-induced ectopic expression, embryos were grown at 28°C using the lines UAS-p35 (Zhou et al, 1997), UAS-bin #35 (Zaffran et al, 2001), byn-GAL4 UAS-GFP (Johansen et al, 2003) (from J. Lengyel, UCLA, USA), bap3-GAL4 (Lee et al, 2003), 2xPE-twi-GAL4;24B-GAL4 (Reim and Frasch, 2005), UAS-HLH54F-IR (P{KK103428}v103965) and UAS-da-IR (P{GD4440}v51300) (both from VDRC, Vienna, Austria) (Dietzl et al, 2007).…”

Section: Drosophila Strainsmentioning

confidence: 99%

HLH54Fis required for the specification and migration of longitudinal gut muscle founders from the caudal mesoderm ofDrosophila

et al. 2010

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SUMMARYHLH54F, the Drosophila ortholog of the vertebrate basic helix-loop-helix domain-encoding genes capsulin and musculin, is expressed in the founder cells and developing muscle fibers of the longitudinal midgut muscles. These cells descend from the posterior-most portion of the mesoderm, termed the caudal visceral mesoderm (CVM), and migrate onto the trunk visceral mesoderm prior to undergoing myoblast fusion and muscle fiber formation. We show that HLH54F expression in the CVM is regulated by a combination of terminal patterning genes and snail. We generated HLH54F mutations and show that this gene is crucial for the specification, migration and survival of the CVM cells and the longitudinal midgut muscle founders. HLH54F mutant embryos, larvae, and adults lack all longitudinal midgut muscles, which causes defects in gut morphology and integrity. The function of HLH54F as a direct activator of gene expression is exemplified by our analysis of a CVM-specific enhancer from the Dorsocross locus, which requires combined inputs from HLH54F and Biniou in a feed-forward fashion. We conclude that HLH54F is the earliest specific regulator of CVM development and that it plays a pivotal role in all major aspects of development and differentiation of this largely twist-independent population of mesodermal cells.

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“…all JAK/STAT functions analysed (Brown et al, 2001;Ghiglione et al, 2002;Johansen et al, 2003), we suspected that it might be forming homo-dimers. To test whether homodimerisation of DOME occurs in Drosophila, and to find how it is controlled during development, we decided to use a technique that would allow us to observe dimerisation in situ.…”

Section: Introductionmentioning

confidence: 99%

Novel level of signalling control in the JAK/STAT pathway revealed by in situ visualisation of protein-protein interaction duringDrosophiladevelopment

Brown

Hombría

2003

Development

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It is commonly accepted that activation of most signalling pathways is induced by ligand receptor dimerisation. This belief has been challenged for some vertebrate cytokine receptors of the JAK/STAT pathway. Here we study whether DOME, the Drosophila receptor of the JAK/STAT pathway, can dimerise and if the dimerisation is ligand-dependent. To analyse DOME homo-dimerisation, we have applied a β-gal complementation technique that allows the detection of protein interactions in situ. This technique has been used previously in cell culture but this is the first time that it has been applied to whole embryos. We show that this technique, which we renameβlue-βlau technique, can be used to detect DOME homo-dimerisation in Drosophila developing embryos. Despite DOME being ubiquitously expressed, dimerisation is developmentally regulated. We investigate the state of DOME dimerisation in the presence or absence of ligand and show that DOME dimerisation is not ligand-induced, indicating that ligand independent cytokine receptor dimerisation is a conserved feature across phyla. We have further analysed the functional significance of ligand-independent receptor dimerisation by comparing the effects of ectopic ligand expression in cells in which the receptor is, or is not, dimerised. We show that ligand expression can only activate STAT downstream targets or affect embryo development in cells in which the receptor is dimerised. These results suggest a model in which ligand-independent dimerisation of the JAK/STAT receptor confers cells with competence to activate the pathway prior to ligand reception. Thus,competence to induce the JAK/STAT signalling pathway in Drosophilacan be regulated by controlling receptor dimerisation prior to ligand binding. These results reveal a novel level of JAK/STAT signalling regulation that could also apply to vertebrates.

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Localized JAK/STAT signaling is required for oriented cell rearrangement in a tubular epithelium

Abstract: SUMMARYLocalized JAK/STAT signaling is required for oriented cell rearrangement in a tubular epithelium

Cited by 68 publications

References 62 publications

Requirement for JAK/STAT signaling throughout border cell migration inDrosophila

Requirement for JAK/STAT signaling throughout border cell migration inDrosophila

HLH54Fis required for the specification and migration of longitudinal gut muscle founders from the caudal mesoderm ofDrosophila

Novel level of signalling control in the JAK/STAT pathway revealed by in situ visualisation of protein-protein interaction duringDrosophiladevelopment

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