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Mutations of thePALB2tumor suppressor gene in humans are associated with hereditary predisposition to breast and also some other cancers. In the present study, we have characterized mice deficient inPalb2. The data show that thePalb2(+/−)mice are normal and fertile, and lack macroscopic tumors when followed up till the age of 8 months. Homozygous (HO)Palb2(−/−)mice present with embryonic lethality and die at E9.5 at the latest. The mutant embryos are smaller in size, developmentally retarded and display defective mesoderm differentiation after gastrulation. InPalb2(−/−)embryos, the expression of cyclin-dependent kinase inhibitorp21is increased, andPalb2(−/−)blastocysts show a growth defectin vitro. Hence, the phenotype of thePalb2(−/−)mice in many regards resembles those previously reported forBrca1andBrca2knockout mice. The similarity in the phenotypes betweenPalb2,Brca1andBrca2knockout mice further supports the functional relationship shownin vitrofor these three proteins. Accordingly, our datain vivosuggest that a key function for PALB2 is to interact with and to build up appropriate communication between BRCA1 and BRCA2, thereby licensing the successful performance of the physiological tasks mediated by these two proteins, particularly in homologous recombination and in proper DNA damage response signaling.

Inactivation of Palb2 gene leads to mesoderm differentiation defect and early embryonic lethality in mice