The formation of functional epithelial tissues involves the coordinated action of several protein complexes, which together produce a cell polarity axis and develop cell-cell junctions. During the last decade, the notion of polarity complexes emerged as the result of genetic studies in which a set of genes was discovered first in Caenorhabditis elegans and then in Drosophila melanogaster. In epithelial cells, these complexes are responsible for the development of the apico-basal axis and for the construction and maintenance of apical junctions. In this review, we focus on apical polarity complexes, namely the PAR3/PAR6/aPKC complex and the CRUMBS/PALS1/PATJ complex, which are conserved between species and along with a lateral complex, the SCRIBBLE/DLG/LGL complex, are crucial to the formation of apical junctions such as tight junctions in mammalian epithelial cells. The exact mechanisms underlying their tight junction construction and maintenance activities are poorly understood, and it is proposed to focus in this review on establishing how these apical polarity complexes might regulate epithelial cell morphogenesis and functions. In particular, we will present the latest findings on how these complexes regulate epithelial homeostasis.
Tuberous sclerosis complex (TSC), caused by dominant mutations in either
TSC1 or
TSC2 tumour
suppressor genes is characterized by the presence of brain malformations, the
cortical tubers that are thought to contribute to the generation of
pharmacoresistant epilepsy. Here we report that tuberless heterozygote
Tsc1+/− mice show
functional upregulation of cortical GluN2C-containing N-methyl-D-aspartate receptors (NMDARs) in an
mTOR-dependent manner and exhibit recurrent, unprovoked seizures during early
postnatal life (
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