[Neurosurgical Embryology. Part 3: Molecular control of corpus callosum development].
The corpus callosum is the most important cerebral commissure allowing axonal fibres to cross the midline. Corpus callosum agenesis is an important condition in man that can reveal numerous genetic syndromes. The corpus callosum develops from the commissural plate, a dorsal region of the telencephalon. Then, axons growing from pyramidal neurons of cortical layer III extend and cross the midline. In experimental models, it is possible to decipher two conditions in which the development of the corpus callosum is impaired. The first condition is characterized by an impairment of the formation of the roof of the telencephalon (the primordium of the commissural plate). This condition can be explained by an abortive induction of this region by an impairment of BMP signaling. This can generate all the forms of holoprosencephaly. Other forms are due to a defective gene coding Hesx1, a transcription factor involved in the control of telencephalic morphogenesis. Such a genetic defect can be observed in human dominant forms of septo-optic dysplasia. The second condition is explained by an impairment of the molecular control of axon growth: such is the case for the couple netrin 1 and DCC or for the adhesion molecule L1.
Catala
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Laboratoire d'Histologie et Embryologie et UMR CNRS 7000, Faculté de Médecine Pitié-Salpêtrière--Université Paris 6. catala@ext.jussieu.fr
D061085:Agenesis of Corpus Callosum; D000818:Animals; D001369:Axons / Q000502:physiology; D051792:Basic Helix-Loop-Helix Proteins; D015815:Cell Adhesion Molecules / Q000235:genetics; D015816:Cell Adhesion Molecules, Neuronal / Q000235:genetics; D058969:Contactin 2; D003337:Corpus Callosum / Q000166:cytology / Q000196:embryology; D029721:Drosophila Proteins; D004626:Embryology / Q000379:methods*; D036342:Ephrins / Q000235:genetics; D016163:Genes, DCC / Q000235:genetics; D018398:Homeodomain Proteins / Q000235:genetics; D006801:Humans; D039841:Leukocyte L1 Antigen Complex / Q000235:genetics; D051379:Mice; D009414:Nerve Growth Factors / Q000235:genetics; D009419:Nerve Tissue Proteins / Q000235:genetics; D000075388:Netrin-1; D009479:Neuropeptides / Q000235:genetics; D009493:Neurosurgery / Q000379:methods*; D012097:Repressor Proteins; D000072056:Transcription Factor HES-1; D014157:Transcription Factors / Q000235:genetics; D025521:Tumor Suppressor Proteins; D000099260:Empty Spiracles Homeobox Proteins
D051792:Basic Helix-Loop-Helix Proteins; D015815:Cell Adhesion Molecules; D015816:Cell Adhesion Molecules, Neuronal; D058969:Contactin 2; D029721:Drosophila Proteins; D036342:Ephrins; D018398:Homeodomain Proteins; D039841:Leukocyte L1 Antigen Complex; D009414:Nerve Growth Factors; D009419:Nerve Tissue Proteins; D000075388:Netrin-1; D009479:Neuropeptides; D012097:Repressor Proteins; D000072056:Transcription Factor HES-1; D014157:Transcription Factors; D025521:Tumor Suppressor Proteins; D000099260:Empty Spiracles Homeobox Proteins; C548674:CNTN2 protein, human; C548675:Cntn2 protein, mouse; C489736:HESX1 protein, human; C489734:Hes1 protein, mouse; C489733:Hesx1 protein, mouse; C000617351:NTN1 protein, human; C000617353:Ntn1 protein, mouse; C485177:Vax1 protein, mouse; C066819:sli protein, Drosophila; C078493:HES1 protein, human