this report provides a single observation which challenges the role of Pygo/Bcl9 interaction in regulating Wnt signaling during development. The sufficiency of a greatly weakened interaction for development and viability challenges its requirement as documented by previous studies. Whether the remaining low interaction is important, whether other parts of the deleted domain in previous studies may play yet unknown roles, and how Wnt signaling is affected in the reported mutant are interesting future questions.
The authors should report numbers when they describe "that mice homozygous for the Pygo2-L331A allele are born in a Mendelian ratio, reach adulthood without any malformation, and are fertile. The Pygo2-L331A mutant allele is also viable when brought into a Pygo1-knockout background (Pygo-/-; Pygo2L331A/L331A), ruling out any compensatory mechanism due to redundancy with Pygo1". How many embryos were scored to back the Mendelian ratio? How many were tested for fertility? How many were brought into the knockout background?