Retarded growth of the medial septum: a major gene effect in acallosal mice.

Absence of the corpus callosum is a hereditary brain defect that appears with varying severity in four inbred mouse strains and is the result of more than one major genetic locus. If relatively few, perhaps two or three, loci are involved in the prenatal ontogeny of the abnormal corpus callosum, it should be possible to identify a distinct morphological process which shows a major gene effect. Because available evidence suggests the source of callosal agenesis occurs in the substrates of axon guidance near the midsagittal plane rather than in the axons themselves, morphometric analysis was done for sagittal sections of the medial septal region in embryos of normal hybrids and four acallosal strains. The anterodorsal zone of the medial septum subadjacent to the cavum septi grew much slower in acallosal BALB/c and I/LnJ mice whereas the ventral septal region was apparently normal. In the Bailey recombinant inbred strains derived from an acallosal BALB/c progenitor, one recombinant (CXBG/By) closely resembled BALB/c whereas the others resembled the normal C57BL/6 parent strain. This pattern of results supports a major gene influence on fusion of the cerebral hemispheres near the region where the corpus callosum first crosses midplane over the dorsal septum.