Department of Biological Sciences, Tata Institute of Fundamental Research, Colaba, Mumbai 400005, India.
SASTRA University, Tirumalaisamudram, Thanjavur 613402, India.
Nat Commun. 2016 Jun 1;7:11643. doi: 10.1038/ncomms11643.
Epithelial cells exhibit apical membrane protrusions, which confer specific functions to epithelial tissues. Microridges are short actin protrusions that are laterally long and form a maze-like pattern in the apical domain. They are widely found on vertebrate squamous epithelia including epidermis and have functions in mucous retention, membrane storage and abrasion resistance. It is largely unknown how the formation of these laterally long actin projections is regulated. Here, we show that antagonistic interactions between aPKC and Lgl-regulators of apical and basolateral domain identity, respectively,-control the length of microridges in the zebrafish periderm, the outermost layer of the epidermis. aPKC regulates the levels of Lgl and the active form of non-muscle myosinII at the apical cortex to prevent actin polymerization-dependent precocious fusion and elongation of microridges. Our data unravels the functional significance of exclusion of Lgl from the apical domain in epithelial cells.
上皮细胞表现出顶端膜突起，赋予上皮组织特定的功能。微脊是短的肌动蛋白突起，侧向较长，并在顶端区域形成迷宫样图案。它们广泛存在于包括表皮在内的脊椎动物鳞状上皮中，在黏液保留、膜储存和抗磨损方面具有功能。目前尚不清楚这些侧向长肌动蛋白突起的形成是如何受到调节的。在这里，我们表明，蛋白激酶 C（aPKC）与 Lgl 之间的拮抗相互作用——分别调节顶端和基底外侧域身份的调节剂——控制斑马鱼表皮最外层的表皮细胞的微脊的长度。aPKC 调节 Lgl 和非肌肉肌球蛋白 II 的活性形式在上皮层中的水平，以防止肌动蛋白聚合依赖性的过早融合和微脊的伸长。我们的数据揭示了在上皮细胞中，Lgl 从顶端区域排除的功能意义。
