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First published online May 10, 2006

Journal of Cell Science 119, 1004e (2006)
© The Company of Biologists Limited
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In this issue

Lgl polarizes the (t)issue


Figure 1

The regulation of epithelial cell polarity is essential for the maintenance and function of many tissues. In Drosophila, the apical PAR-3-aPKC-PAR-6 complex and the basolateral tumour suppressor protein Lgl act antagonistically to regulate epithelial polarity. In mammals, although similar proteins regulate epithelial cell polarity, the exact role of mLgl-1 and mLgl-2, the two mammalian orthologues of Drosophila Lgl, is unclear. On p. 2107 Shigeo Ohno and co-workers provide new insights into this mystery by using RNAi to show that endogenous mLgl is needed for the disassembly of apical membrane domains in a mammalian kidney cell line induced to depolarize by Ca2+ depletion. mLgl proteins, they report, function by suppressing the activity of the apical PAR-3-aPKC-PAR-6 complex and are required in other situations where epithelial cell polarity is manipulated, such as collagen-mediated re-orientation of apical membrane polarity. Given these results, the authors speculate that mLgl helps to ensure that the polarization of individual cells is integrated with whole tissue architecture.


Related articles in JCS:

Lgl mediates apical domain disassembly by suppressing the PAR-3-aPKC-PAR-6 complex to orient apical membrane polarity
Tomoyuki Yamanaka, Yosuke Horikoshi, Natsuko Izumi, Atsushi Suzuki, Keiko Mizuno, and Shigeo Ohno
JCS 2006 119: 2107-2118. [Abstract] [Full Text]  




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