Journal
SCIENTIFIC REPORTS
Volume 8, Issue -, Pages -Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/s41598-018-19579-5
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Funding
- Biotechnology and Biological Science Research Council [BB/J015032/1, BB/N014855/1]
- Moorfields Eye Charity [R170006A]
- Fight for Sight [1740/1741]
- Welcome Trust multiuser equipment grant [099173/Z/12/Z]
- BBSRC [BB/N014855/1, BB/J015032/1, BB/R00627X/1] Funding Source: UKRI
- Biotechnology and Biological Sciences Research Council [BB/J015032/1, BB/R00627X/1, BB/N014855/1] Funding Source: researchfish
- Fight for Sight [1740/41] Funding Source: researchfish
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Tight junctions are required for the formation of tissue barriers and function as suppressors of signalling mechanisms that control gene expression and cell behaviour; however, little is known about the physiological and developmental importance of such signalling functions. Here, we demonstrate that depletion of MarvelD3, a transmembrane protein of tight junctions, disrupts neural crest formation and, consequently, development of neural crest-derived tissues during Xenopus embryogenesis. Using embryos and explant cultures combined with a small molecule inhibitor or mutant mRNAs, we show that MarvelD3 is required to attenuate JNK signalling during neural crest induction and that inhibition of JNK pathway activation is sufficient to rescue the phenotype induced by MarvelD3 depletion. Direct JNK stimulation disrupts neural crest development, supporting the importance of negative regulation of JNK. Our data identify the junctional protein MarvelD3 as an essential regulator of early vertebrate development and neural crest induction and, thereby, link tight junctions to the control and timing of JNK signalling during early development.
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