A successful pregnancy depends on many events, such as the attachment of the allantois to the chorionic mesothelium. However, little is known about the genes that are expressed in the chorionic trophoblast and whose loss results in attachment defects. Mrj, which encodes a co-chaperone, is one of these genes, and is now shown by James Cross and colleagues to regulate the turnover of keratin in the developing mouse placenta (see p. 1809). Chorioallantoic attachment fails and keratin inclusion bodies develop in Mrj-/- embryos. This attachment failure is a consequence of cytotoxicity, the authors show, that is caused by keratin inclusion bodies rather than by a failure of the keratin cytoskeleton to form; keratin-deficient embryos correctly attach, and a reduction in keratin expression in Mrj-/- conceptuses rescues failed attachment. Mrj is known to interact with Huntington disease proteins with expanded N-terminal repeat aggregates within neurons. Because inclusion bodies are associated with other neurodegenerative diseases, the authors propose that Mrj may have a more general role in preventing intracellular inclusion bodies.
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