Maternal Interferon Regulatory Factor 6 is required for the differentiation of primary superficial epithelia in Danio and Xenopus embryos

Sabel, Jaime L.; d'Alençon, Claudia; O’Brien, Erin; Otterloo, Eric Van; Lutz, Katie; Cuykendall, Tawny N.; Schutte, Brian C.; Houston, Douglas; Cornell, Robert A.

doi:10.1016/j.ydbio.2008.10.031

Cited by 60 publications

(87 citation statements)

References 88 publications

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“…Similar time-dependent differences in phenotype have been described for IRF6. 10,11,28 Ectopic expression of WT hRIPK4 rescued the exogastrulation caused by IRF6DBD expression, suggesting that IRF6-dependent gastrulation in Xenopus is mediated, at least in part, through transcriptional regulation of RIPK4. Indeed, we found that IRF6 overexpression transactivated the hRIPK4 promoter.…”

Section: G H and I)mentioning

confidence: 99%

“…10,11 Moreover, similar to RIPK4 activity, IRF6 is also required for gastrulation in Danio rerio and X. laevis. 28 Until now, there is no evidence that functionally connects these two molecules. A hRIPK4 promoter reporter construct was significantly induced by cotransfection of hIRF6 in mammalian cells, showing that RIPK4 can act downstream of IRF6 (Figure 7a).…”

Section: G H and I)mentioning

confidence: 99%

“…Interestingly, it was reported that disruption of gastrulation movements by the expression of IRF6DBD in zebrafish embryos was accompanied by a substantial reduction of cortical actin in the superficial cell layer. 28 Therefore, we performed actin staining on stage 11 animal caps isolated from embryos injected with either RIPK4Mo atg or IRF6DBD RNA. Although control morpholinoinjected animal caps showed high levels of cortical actin in the cells facing the blastocoel, little F-actin was present in similar stage animal caps injected with RIPK4Mo atg or IRF6DBD RNA (Figure 7e).…”

Section: G H and I)mentioning

confidence: 99%

“…28 While splicing-blocking morpholinos only interfere with zygotic expression, translation-blocking morpholinos also target maternal transcripts, which could explain the observed phenotypic differences. Similar time-dependent differences in phenotype have been described for IRF6.…”

Section: G H and I)mentioning

confidence: 99%

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A novel RIPK4–IRF6 connection is required to prevent epithelial fusions characteristic for popliteal pterygium syndromes

et al. 2014

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Receptor-interacting protein kinase 4 (RIPK4)-deficient mice have epidermal defects and fusion of all external orifices. These are similar to Bartsocas-Papas syndrome and popliteal pterygium syndrome (PPS) in humans, for which causative mutations have been documented in the RIPK4 and IRF6 (interferon regulatory factor 6) gene, respectively. Although genetically distinct, these syndromes share the anomalies of marked pterygia, syndactyly, clefting and hypoplastic genitalia. Despite the strong resemblance of these two syndromes, no molecular connection between the transcription factor IRF6 and the kinase RIPK4 was known and the mechanism underlying the phenotype was unclear. Here we describe that RIPK4 deficiency in mice causes epithelial fusions associated with abnormal periderm development and aberrant ectopic localization of E-cadherin on the apical membrane of the outer peridermal cell layers. In Xenopus, RIPK4 depletion causes the absence of ectodermal epiboly and concomitant gastrulation defects that phenocopy ectopic expression of dominant-negative IRF6. We found that IRF6 controls RIPK4 expression and that wild-type, but not kinase-dead, RIPK4 can complement the gastrulation defect in Xenopus caused by IRF6 malfunctioning. In contrast to the mouse, we observed only minor effects on cadherin membrane expression in Xenopus RIPK4 morphants. However, gastrulation defects were associated with a virtual absence of cortical actin in the ectodermal cells that face the blastocoel cavity and this was phenocopied in embryos expressing dominant-negative IRF6. A role for RIPK4 in actin cytoskeleton organization was also revealed in mouse epidermis and in human epithelial HaCaT cells. In conclusion, we showed that in mice RIPK4 is implicated in cortical actin organization and in E-cadherin localization or function, which can explain the characteristic epithelial fusions observed in PPSs. In addition, we provide a novel molecular link between IRF6 and RIPK4 that unifies the different PPSs to a common molecular pathway.

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Section: G H and I)mentioning

confidence: 99%

Section: G H and I)mentioning

confidence: 99%

Section: G H and I)mentioning

confidence: 99%

Section: G H and I)mentioning

confidence: 99%

See 2 more Smart Citations

A novel RIPK4–IRF6 connection is required to prevent epithelial fusions characteristic for popliteal pterygium syndromes

et al. 2014

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“…EVL cell fate must be properly specified for epiboly to proceed normally (Pei et al, 2007;Sabel et al, 2009). For example, simultaneous morpholino knock-down of several EVL-specific intermediate filament genes results in epiboly delay of the EVL, YSL, and deep cells (Pei et al, 2007).…”

Section: Introductionmentioning

confidence: 99%

The tight junction component Claudin E is required for zebrafish epiboly

Siddiqui

Sheikh

Tran

et al. 2010

Developmental Dynamics

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Zebrafish epiboly results in the thinning and spreading of the blastoderm to cover the yolk cell and close the blastopore. The extra-embryonic yolk syncytial layer (YSL) tows the blastoderm vegetally during epiboly by means of its tight junction attachments to the enveloping layer (EVL). Claudins are the major transmembrane protein components of tight junctions. Here, we focus on the function of Claudin E (Cldne), which is expressed specifically in the EVL. Morpholino knock-down of cldne produced a highly penetrant epiboly delay. Our analysis suggested that the EVL margin, which is attached to the YSL, was under reduced tension in morphant embryos. We propose that local variation in the strength of EVL-YSL attachment in morphant embryos resulted in slow and uneven advancement of the EVL and blastoderm. Our work is the first to demonstrate that Claudins are important for zebrafish epiboly. Developmental Dynamics 239:715-722,

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