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Here we describe the axonal defects of <jats:italic>baffled<\/jats:italic> in further detail and identify a point mutation in the <jats:italic>Hspa5<\/jats:italic> gene, encoding the endoplasmic reticulum chaperone BiP\/GRP78. This hypomorphic mutation of BiP disrupts proper development of the thalamocortical axon projection and other forebrain axon tracts, as well as cortical lamination. In <jats:italic>baffled<\/jats:italic> mutant brains, a reduced number of thalamic axons innervate the cortex by the time of birth. Thalamocortical and corticothalamic axons are delayed, overfasciculated, and disorganized along their pathway through the ventral telencephalon. Furthermore, dissociated mutant neurons show reduced axon extension in vitro. Together, these findings demonstrate a sensitive requirement for the endoplasmic reticulum chaperone BiP\/GRP78 during axon outgrowth and pathfinding in the developing mammalian brain. J. Comp. Neurol. 521:677\u2013696, 2013. \u00a9 2012 Wiley Priodcals, Inc.<\/jats:p>","DOI":"10.1002\/cne.23199","type":"journal-article","created":{"date-parts":[[2012,7,23]],"date-time":"2012-07-23T10:05:26Z","timestamp":1343037926000},"page":"677-696","source":"Crossref","is-referenced-by-count":21,"title":["Mutation of the BiP\/GRP78 gene causes axon outgrowth and fasciculation defects in the thalamocortical connections of the mammalian forebrain"],"prefix":"10.1002","volume":"521","author":[{"given":"Carlita B.","family":"Favero","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Rasha N.","family":"Henshaw","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Cynthia 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