ArticleDevelopment (Cambridge, England)2026
Loss of Twist impairs tentacle development and induces epithelial neoplasia in the sea anemone Nematostella vectensis.
Article in Development (Cambridge, England), 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
1 citing paper in PubMed.
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Authors and funding
7 authors.
Funding
Abstract
Appendages are key features of the body plans of arthropods and vertebrates, yet little is known about appendage formation outside of bilaterians. Here, we investigate the molecular regulation underlying the formation of tentacles, the appendages in cnidarians. We find that the bHLH transcription factor Twist plays a crucial role in tentacle morphogenesis and tissue homeostasis in the sea anemone Nematostella vectensis. Using CRISPR/Cas9, we show that twist mutants exhibit impaired secondary tentacle formation, delayed and reduced proliferation in budding tentacles, and the absence of microcnemes, structures that demarcate tentacle boundaries, suggesting defects in spatial patterning. Loss of Twist disrupts expression of co-expressed mesodermal transcription factors paraxis and tbx15 and perturbs the TOR-FGF signalling feedback loop necessary for normal tentacle growth. We note that the link of Twist and FGF signalling is reminiscent of limb formation in vertebrates. Moreover, starting at juveniles, mutants develop neoplasm-like epithelial overgrowth with tentacle-like molecular profiles, indicating a role for Twist in maintaining tissue homeostasis at the oral pole. Together, Twist integrates major signalling pathways to regulate secondary tentacle patterning and maintain spatial tissue organisation in the diploblastic N. vectensis.
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