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The Wnt pathway 2

Part 2 of 2
Published on September 30, 2024   48 min

Other Talks in the Series: The Molecular Basis of Cancer

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0:04
Welcome back from the break. We're now going to talk about, how does Wnt signal?
0:11
We understood a lot about the genes in the Wnt pathway from flies. Where we saw porcupine, wntless, frizzled, dishevelled, zeste-white 3, armadillo, and Tcf. When it became clear that it is also important in cancer, there's a lot of interest in looking at it in the human system. Then it turned out that there was a very good alignment between flies and mammals. Flies have wingless, humans have Wnt. Same gene, different names. Then there's frizzled, dishevelled, a kinase which in vertebrates is GSK3, β-catenin, and then the transcriptional repressor Tcf/Lef leading to β-catenin regulated transcription.
1:00
In its basic form, Wnt/β-catenin signaling is pretty simple. I've already told you, Wnt bind to receptors at the cell surface that sets up a signaling cascade that stabilizes the β-catenin protein which then moves to the nucleus and turns on important genes. That's a really simple model. Of course, it's never that simple. We call this simple model the canonical pathway.
1:27
This simple model has a few more details, where you can see GSK3, Casein kinase 1α, Axin, APC, and β-catenin form a complex in the cytoplasm. This complex has been called the β-catenin destruction complex because that's its job—to cause degradation of β-catenin that has left the membrane. Now, I told you the Wnt pathway is simple and the canonical view of the pathway is indeed simple but life is complicated.

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