We are doing well and it's definitely neat to have a UT reunion here many years down the road!

On a final note, we would like to thank our reviewers for their enthusiasm about this work and for their experimental and analytical suggestions which significantly strengthened this study.

Thus, Wnt activity levels must be modulated throughout cranial neural tube closure in order to control both proliferation and cell remodeling in order for closure to complete.

Conversely, conditional inactivation of APC and resulting hyperactivation of Wnt signaling, leads to apical constriction blockade by altering actin organization, and this occurs without changes in proliferation or tissue scaling.

Loss of robust Wnt signaling in Lrp6 mutants drives an early burst of excessive cell proliferation in the cranial tissues, leading to a doubling of the tissue volume and width. This excessive width blocks closure despite the normal function of cell remodeling programs, including apical constriction.

In this study we find that either hypomorphic or hypermorphic Wnt signaling states lead to cranial neural tube closure defects, but interestingly the underlying cellular defects in pathway activity states are distinct.

Together, these analyses suggest that Wnt activity levels must be strictly modulated to tune both tissue scaling and curvature change during cranial closure.

On the other hand, hyperactivation of Wnt signaling by conditional inactivation of APC specifically in the cranial folds blocks apical constriction, preventing neural fold elevation.

We find that reduced Wnt signaling in Lrp6 mutants leads to a surprising tissue hyperplasia phenotype in the cranial neural plate, which leads to a doubling of tissue width, preventing closure. This hyperplasia is driven by an early doubling of proliferation specifically in anterior cranial tissues