FOREBRAIN AND MIDBRAIN REGIONS ARE DELETED IN OTX2(- -) MUTANTS DUE TO A DEFECTIVE ANTERIOR NEUROECTODERM SPECIFICATION DURING GASTRULATION/

We have replaced part of the mouse homeogene Otx2 coding region with t he E. coli lacZ coding sequence, thus creating a null allele of Otx2. By 9.5 dpc, homozygous mutant embryos are characterized by the absence of forebrain and midbrain regions. From the early to mid-streak stage s, endomesodermal cells expressing lacZ fail to be properly localized anteriorly. In the ectodermal layer, lacZ transcription is progressive ly extinguished, being barely detectable by the late streak stage. The se data suggest that Otx2 expression in endomesoderm and ectoderm is r equired for anterior neuroectoderm specification. In gastrulating hete rozygous embryos, a post-transcriptional repression acts on lacZ trans cripts in the ectoderm, but not in the external layer, suggesting that different post-transcriptional mechanisms control Otx2 expression in both layers.