Endoplasmic reticulum stress induced by tunicamycin disables germ layer formation in <i>Xenopus laevis</i> embryos

Li, Yuan; Cao, Ying; Knöchel, Walter

doi:10.1002/dvdy.21299

Cited by 8 publications

(8 citation statements)

References 32 publications

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“…This response is orchestrated by several sensing mechanisms and finally transmitted to the nucleus in the form of activated transcription factors Xbp1 and members of the ATF/Creb family (Calfon et al, 2002;Haze et al, 1999;Kondo et al, 2005;Kondo et al, 2007;Yoshida et al, 2001). Xbp1 has previously been identified in Xenopus embryos and shown to have a role in regulating BMP signaling, in mesoderm formation, and in the response of the embryo to ER stress (Cao et al, 2006;Yuan et al, 2007;Yuan et al, 2008;Zhao et al, 2003). We find that xbp1 and at least one Creb family gene, creb3l2, are preferentially expressed in the notochord and are required for notochord differentiation.…”

Section: Introductionmentioning

confidence: 60%

“…Thus the inhibition of expression of Xbp1 or Creb3l2 leads to an impairment of notochord morphology by tailbud stages of embryogenesis. Manipulation of Xbp1 and Creb3l2 protein levels affects the expression of some secretory protein genes Xbp1 is known to have a role in Xenopus embryogenesis (Cao et al, 2006;Yuan et al, 2008;Zhao et al, 2003) and to be involved in the response to ER stress (Yuan et al, 2007). We tested whether inhibition of Xbp1 or Creb3l2 affects the expression of secretory pathway genes at early and later stages of notochord differentiation.…”

Section: Requirement For Xbp1 and Creb3l2 In Notochord Developmentmentioning

confidence: 99%

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Coordinated activation of the secretory pathway during notochord formation in theXenopusembryo

et al. 2009

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We compared the transcriptome in the developing notochord of Xenopus laevis embryos with that of other embryonic regions. A coordinated and intense activation of a large set of secretory pathway genes was observed in the notochord, but not in notochord precursors in the axial mesoderm at early gastrula stage. The genes encoding Xbp1 and Creb3l2 were also activated in the notochord. These two transcription factors are implicated in the activation of secretory pathway genes during the unfolded protein response, where cells react to the stress of a build-up of unfolded proteins in their endoplasmic reticulum. Xbp1 and Creb3l2 are differentially expressed but not differentially activated in the notochord. Reduction of expression of Xbp1 or Creb3l2 by injection of antisense morpholinos led to strong deficits in notochord but not somitic muscle development. In addition, the expression of some, but not all, genes encoding secretory proteins was inhibited by injection of xbp1 morpholinos. Furthermore, expression of activated forms of Xbp1 or Creb3l2 in animal explants could activate a similar subset of secretory pathway genes. We conclude that coordinated activation of a battery of secretory pathway genes mediated by Xbp1 and Creb/ATF factors is a characteristic and necessary feature of notochord formation.

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Section: Introductionmentioning

confidence: 60%

Section: Requirement For Xbp1 and Creb3l2 In Notochord Developmentmentioning

confidence: 99%

Coordinated activation of the secretory pathway during notochord formation in theXenopusembryo

et al. 2009

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“…TM is the inducer of UPR, and it was reported that TM induced severe ER stress with an apparent increase in XBP1 splicing and caused serious developmental defects in Xenopus [19]. We speculated that, if XBP1 splicing is repressed, the developmental defects could be rescued.…”

Section: Resultsmentioning

confidence: 95%

“…In parallel, ODC was amplified to confirm equal amounts and integrity of different RNA preparations. Real time RT-PCR was performed and primers for chop were as described previously[19].…”

Section: Methodsmentioning

confidence: 99%

IRE1a knockdown rescues tunicamycin-induced developmental defects and apoptosis in Xenopus laevis

Li¹,

Yü²,

Li³

et al. 2014

J Biomed Res

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Inositol requiring enzyme-1 (IRE1) is highly conserved from yeasts to humans. Upon endoplasmic reticulum (ER) stress, IRE1 activates X-box-binding protein 1 (XBP1) by unconventional splicing of XBP1 mRNA, which activates unfolded protein response (UPR) to restore ER homeostasis. In mice, IRE1α plays an essential role in extraembryonic tissues. However, its precise action during the early stage of development is unknown. In this study, the gain and loss-of-function analyses were used to investigate the function of Xenopus IRE1α (xIRE1α). The effects of xIRE1α during embryo development were detected with RT-PCR and whole mount in situ hybridization. ER stress was induced by tunicamycin. The apoptotic cells were measured by TUNNEL assays. Although both gain and loss of xIRE1α function had no significant effect on Xenopus embryogenesis, knockdown of xIRE1α could rescue tunicamycin-induced developmental defects and apoptosis. The finding indicates that xIRE1α is not required for embryogenesis but is required for tunicamycin-induced developmental defects and apoptosis in Xenopus laevis.

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“…TUNI triggers stress by inhibiting N-linked glycosylation of newly synthesized proteins in the ER [41]. Glycosylation is essential for controlling both the processing and quality of protein folding.…”

Section: Tuni and Ersmentioning

confidence: 99%

Crosstalk Between Nuclear Glucose-Regulated Protein 78 and Tumor Protein 53 Contributes to the Lipopolysaccharide Aggravated Apoptosis of Endoplasmic Reticulum Stress-Responsive Porcine Intestinal Epithelial Cells

Jiang¹,

Liu²,

Chen³

et al. 2018

Cell Physiol Biochem

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Background/Aims: Lipopolysaccharides (LPSs) act as virulence factors that trigger intestinal inflammation and thereby compromise the production of pigs worldwide. Intestinal diseases and dysfunction have been attributed to endoplasmic reticulum stress (ERS) and the subsequent apoptosis of intestinal epithelial cells. Therefore It is important to explore whether LPSs aggravate ERS-mediated apoptosis of intestinal epithelial cells. Methods: ERS and inflammation models were established in porcine cell line J2 (IPEC-J2) and the cells were treated with tunicamycin or LPS at specific times. The expression of marker proteins was determined by western blot and immunofluorescence. Possible crosstalk between proteins was analyzed by co-immunoprecipitation. Small interfering RNA transfection was employed to verify the mechanisms. Results: We found that Escherichia coli-derived LPS aggravated ERS and ERS-mediated apoptosis in ERS-responsive IPEC-J2 cells. The crosstalk between nuclear glucose-regulated protein 78 (GRP78) and tumor protein 53 (p53) was verified to trigger this LPS-aggravated apoptosis of ERS-responsive intestinal cells. Conclusion: This novel finding implies that intestinal malfunctions might solely originate from the effects of Gram-negative bacteria on ERS-responsive intestinal cells. The regulation of ERS signaling (especially the crosstalk between nuclear GRP78 and p53) in ERS-responsive/rapidly growing intestines may help intestinal cells survive from Gram-negative bacterial infections.

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Endoplasmic reticulum stress induced by tunicamycin disables germ layer formation in Xenopus laevis embryos

Abstract: Maintenance of endoplasmic reticulum (ER) homeostasis is

Cited by 8 publications

References 32 publications

Coordinated activation of the secretory pathway during notochord formation in theXenopusembryo

Coordinated activation of the secretory pathway during notochord formation in theXenopusembryo

IRE1a knockdown rescues tunicamycin-induced developmental defects and apoptosis in Xenopus laevis

Crosstalk Between Nuclear Glucose-Regulated Protein 78 and Tumor Protein 53 Contributes to the Lipopolysaccharide Aggravated Apoptosis of Endoplasmic Reticulum Stress-Responsive Porcine Intestinal Epithelial Cells

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