NMII forms a contractile transcellular sarcomeric network to regulate apical cell junctions and tissue geometry.

Thursday, November 07, 2013 — Poster Session II
12:00 p.m. – 2:00 p.m.	FAES Academic Center (Upper-Level Terrace)	NIDCD	CHEMCELL-7

Authors

S Ebrahim
T Fujita
BA Millis
E Kozin
X Ma
S Kawamoto
MA Baird
M Davidson
S Yonemura
Y Hisa
MA Conti
RS Adelstein
H Sakaguchi
B Kachar

Abstract

A belt comprised of actin and non-muscle myosin II (NMII) filaments circumscribes the inner surface of the epithelial cells adjacent to the junctions where cell-cell contacts are maintained. NMII within this belt is thought to be the master integrator of force mediating epithelial morphognesis and tensional homeostasis. Unsurprisingly, mutations in NMII are associated with a number of diseases. However, how NMII is organized within the actin belt to generate contractility along the junctional line remains unknown, and current models depict a random arrangement of NMII at the level of the adherens junction. Here we reveal an unexpected, highly ordered complexity within the epithelial apical junctional belt. Periodic assemblies of bipolar NMII filaments interlace with perijunctional actin and α-actinin to form mini-sarcomeres arranged end-to-end in a continuous, muscle-like contractile belt around each epithelial cell. Remarkably, the sarcomeres of adjacent cells are paired, and maintain register, across the junctional line forming an integrated, transcellular contractile network. The contraction/relaxation of paired sarcomeres concomitantly impacts changes in apical cell shape and tissue geometry. Our results provide a model for how NMII force generation is effected along the junctional perimeter of individual cells, and communicated across neighboring cells in epithelial sheets.