title: Biological adhesion of the flatworm Macrostomum lignano relies on a duo-gland system and is mediated by a cell type-specific intermediate filament protein.
abstract: BACKGROUND
  Free-living flatworms, in both marine and freshwater environments, are able to adhere to and release from a substrate several times within a second. This reversible adhesion relies on adhesive organs comprised of three cell types: an adhesive gland cell, a releasing gland cell, and an anchor cell, which is a modified epidermal cell responsible for structural support. However, nothing is currently known about the molecules that are involved in this adhesion process.
  
  
  RESULTS
  In this study we present the detailed morphology of the adhesive organs of the free-living marine flatworm Macrostomum lignano. About 130 adhesive organs are located in a horse-shoe-shaped arc along the ventral side of the tail plate. Each organ consists of exactly three cells, an adhesive gland cell, a releasing gland cell, and an anchor cell. The necks of the two gland cells penetrate the anchor cell through a common pore. Modified microvilli of the anchor cell form a collar surrounding the necks of the adhesive- and releasing glands, jointly forming the papilla, the outer visible part of the adhesive organs. Next, we identified an intermediate filament (IF) gene, macif1, which is expressed in the anchor cells. RNA interference mediated knock-down resulted in the first experimentally induced non-adhesion phenotype in any marine animal. Specifically, the absence of intermediate filaments in the anchor cells led to papillae with open tips, a reduction of the cytoskeleton network, a decline in hemidesmosomal connections, and to shortened microvilli containing less actin.
  
  
  CONCLUSIONS
  Our findings reveal an elaborate biological adhesion system in a free-living flatworm, which permits impressively rapid temporary adhesion-release performance in the marine environment. We demonstrate that the structural integrity of the supportive cell, the anchor cell, is essential for this adhesion process: the knock-down of the anchor cell-specific intermediate filament gene resulted in the inability of the animals to adhere. The RNAi mediated changes of the anchor cell morphology are comparable to situations observed in human gut epithelia. Therefore, our current findings and future investigations using this powerful flatworm model system might contribute to a better understanding of the function of intermediate filaments and their associated human diseases.
authors: Birgit
authors: B
authors: Lengerer
authors: Robert
authors: R
authors: Pjeta
authors: Julia
authors: J
authors: Wunderer
authors: Marcelo
authors: M
authors: Rodrigues
authors: Roberto
authors: R
authors: Arbore
authors: Lukas
authors: L
authors: Schärer
authors: Eugene
authors: E
authors: Berezikov
authors: Michael W
authors: MW
authors: Hess
authors: Kristian
authors: K
authors: Pfaller
authors: Bernhard
authors: B
authors: Egger
authors: Sabrina
authors: S
authors: Obwegeser
authors: Willi
authors: W
authors: Salvenmoser
authors: Institute of Zoology and Center of Molecular Bioscience Innsbruck, University of Innsbruck, Technikerstr, 25, Innsbruck A-6020, Austria. peter.ladurner@uibk.ac.at.
authors: Peter
authors: P
authors: Ladurner