On the cover
When the tumor suppressor Lkb1 is inhibited in explants of embryonic pancreas, epithelial structures that resemble precancerous lesions are formed even though cell polarity—indicated by actin (red) and the basolateral marker EpCAM (green)—remains intact. Lo et al. use chemical genetics and ex vivo cultures to identify distinct Lkb1-dependent pathways in tissue morphogenesis and cancer development.
Image © 2012 Lo et al.
See page 1117.
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In vivo imaging reveals that CSB and XPC promote the repair of oxidative DNA lesions independent of the canonical nucleotide excision repair process.
The Golgi resident protein Cab45 is required for trans-Golgi network Ca2+ homeostasis and sorting of cargos that are destined for secretion.
The chromatin remodeling enzyme p400 forms a complex with Rad51 and is required for its recruitment to double-strand breaks during DNA repair by homologous recombination.
Cep164 provides a molecular link between the mother centriole and the ciliary membrane biogenesis machinery by interacting with the GEF Rabin8 and the GTPase Rab8.
VEGF causes translocation of Syx from endothelial cell junctions, promoting junction disassembly, whereas Angtiopoietin-1 maintains Syx at the junctions and stabilizes them.
A combination of ex vivo embryonic tissue culture, genetic manipulation, and chemical genetics reveals novel details of Lkb1-mediated regulation of tissue morphogenesis.
Tao initiates morphogenesis of a squamous epithelium by promoting the endocytosis of the adhesion molecule Fasciclin 2 from the lateral membrane.
Plasma membrane calcium ATPase regulates bone mass by fine-tuning osteoclast differentiation and survival
Plasma membrane calcium ATPases PMCA1 and PMCA4 regulate osteoclast differentiation and survival by regulating NFATc1 and NO.