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First published online January 12, 2006

Journal of Cell Science 119, 201e (2006)
© The Company of Biologists Limited
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In this issue

Nuclear organization: a titin-ic task


The nuclei of cells in multicellular animals are supported by a network of lamin filaments. Lamin mutations cause numerous laminopathies, each of which affects a different tissue. One explanation for this disease pattern is that lamins interact with tissue-specific binding partners. Katherine Wilson and colleagues have used two-hybrid analysis to identify an unexpected binding partner for lamin: titin (p. 239). Cytoplasmic isoforms of this enormous protein organize muscle sarcomeres; in non-muscle cells, titin is essential for chromosome condensation and segregation during mitosis. Wilson's team now reveals that titin also helps to organize the nucleus during interphase through the interaction of its C-terminus with lamins. They show that the interphase localization of titin depends on lamin in Caenorhabditis elegans embryos and that nuclear lamina integrity and nuclear architecture are disrupted by overexpression of lamin-binding fragments of titin in mammalian cells. The authors speculate that the cellular phenotypes that underlie different laminopathies reflect the combined loss of lamins and other structural proteins that together determine nuclear structure.


Related articles in JCS:

Nuclear Titin interacts with A- and B-type lamins in vitro and in vivo
Michael S. Zastrow, Denise B. Flaherty, Guy M. Benian, and Katherine L. Wilson
JCS 2006 119: 239-249. [Abstract] [Full Text]  




This Article
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