We have investigated the embryonic processes that require huntingtin in order to more precisely delineate huntingtin's essential molecular and cellular activities and to provide clues to the mechanism by which the dominant polyglutamine expansion mutation in huntingtin leads to HD pathogenesis. In pursuing the finding that huntingtin is needed only in extraembryonic tissues for normal gastrulation, our data fail to provide evidence of abnormal nutritive gene expression in Hdhex4/5/Hdhex4/5 embryos. Instead, our results reveal that huntingtin is required for normal anterior streak formation and the consequent production of paraxial mesoderm, with a previously unrecognized role for huntingtin in the proper extinction of transiently and/or dynamically expressed genes.