Mutational analysis supports a core role for Drosophila α-Catenin in adherens junction function

R Sarpal, M Pellikka, RR Patel, FYW Hui… - Journal of cell …, 2012 - journals.biologists.com
R Sarpal, M Pellikka, RR Patel, FYW Hui, D Godt, U Tepass
Journal of cell science, 2012journals.biologists.com
α-catenin associates the cadherin–catenin complex with the actin cytoskeleton. α-catenin
binds to β-catenin, which links it to the cadherin cytoplasmic tail, and F-actin, but also to a
multitude of actin-associated proteins. These interactions suggest a highly complex cadherin–
actin interface. Moreover, mammalian αE-catenin has been implicated in a cadherin-
independent cytoplasmic function in Arp2/3-dependent actin regulation, and in cell
signaling. The function and regulation of individual molecular interactions of α-catenin, in …
α-catenin associates the cadherin–catenin complex with the actin cytoskeleton. α-catenin binds to β-catenin, which links it to the cadherin cytoplasmic tail, and F-actin, but also to a multitude of actin-associated proteins. These interactions suggest a highly complex cadherin–actin interface. Moreover, mammalian αE-catenin has been implicated in a cadherin-independent cytoplasmic function in Arp2/3-dependent actin regulation, and in cell signaling. The function and regulation of individual molecular interactions of α-catenin, in particular during development, are not well understood. We have generated mutations in Drosophila α-Catenin (α-Cat) to investigate α-Catenin function in this model, and to establish a setup for testing α-Catenin-related constructs in α-Cat-null mutant cells in vivo. Our analysis of α-Cat mutants in embryogenesis, imaginal discs and oogenesis reveals defects consistent with a loss of cadherin function. Compromising components of the Arp2/3 complex or its regulator SCAR ameliorate the α-Cat loss-of-function phenotype in embryos but not in ovaries, suggesting negative regulatory interactions between α-Catenin and the Arp2/3 complex in some tissues. We also show that the α-Cat mutant phenotype can be rescued by the expression of a DE-cadherin::α-Catenin fusion protein, which argues against an essential cytosolic, cadherin-independent role of Drosophila α-Catenin.
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