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During brain development CC forms at the boundary area between the cortex and the septum and special transient neural and glial guidepost structures in this area are thought to be critical for CC formation. In addition, it is thought that the fusion of the two hemispheres in the septum area is a prerequisite for CC formation. However, very little is known of the molecular mechanisms behind the fusion of the two hemispheres. Netrin1 (NTN1) acts as an axon guidance molecule in the developing central nervous system and <jats:italic>Ntn1<\/jats:italic> deficiency leads to the agenesis of CC in mouse. Here we have analyzed <jats:italic>Ntn1<\/jats:italic> deficient mice to better understand the reasons behind the observed lack of CC. We show that <jats:italic>Ntn1<\/jats:italic> deficiency leads to defects in neural, but not in glial guidepost structures that may contribute to the agenesis of CC. In addition, <jats:italic>Nnt1<\/jats:italic> was expressed by the leptomeningeal cells bordering the two septal walls prior to fusion. Normally these cells are removed when the septal fusion occurs. At the same time, the Laminin containing basal lamina produced by the leptomeningeal cells is disrupted in the midline area to allow the cells to mix and the callosal axons to cross. In <jats:italic>Ntn1<\/jats:italic> deficient embryos however, the leptomeninges and the basal lamina were not removed properly from the midline area and the septal fusion did not occur. Thus, NTN1 contributes to the formation of the CC by promoting the preceding removal of the midline leptomeningeal cells and interhemispheric fusion.<\/jats:p>","DOI":"10.1016\/j.ijdevneu.2015.08.005","type":"journal-article","created":{"date-parts":[[2015,10,23]],"date-time":"2015-10-23T14:05:06Z","timestamp":1445609106000},"page":"206-215","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":14,"title":["Defects in neural guidepost structures and failure to remove leptomeningeal cells from the septal midline behind the interhemispheric fusion defects in <i>Netrin1<\/i> deficient mice"],"prefix":"10.1002","volume":"47","author":[{"given":"Janne","family":"Hakanen","sequence":"first","affiliation":[{"name":"Department of Veterinary Biosciences University of Helsinki Finland"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Marjo","family":"Salminen","sequence":"additional","affiliation":[{"name":"Department of Veterinary Biosciences University of Helsinki Finland"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"311","published-online":{"date-parts":[[2015,10,22]]},"reference":[{"key":"e_1_2_7_2_1","doi-asserted-by":"publisher","DOI":"10.1016\/j.brainresrev.2004.11.003"},{"key":"e_1_2_7_3_1","doi-asserted-by":"publisher","DOI":"10.1371\/journal.pgen.1002606"},{"key":"e_1_2_7_4_1","doi-asserted-by":"publisher","DOI":"10.1242\/dev.127.22.4891"},{"key":"e_1_2_7_5_1","doi-asserted-by":"publisher","DOI":"10.1101\/gad.1807209"},{"key":"e_1_2_7_6_1","doi-asserted-by":"publisher","DOI":"10.1016\/j.neuron.2011.11.036"},{"key":"e_1_2_7_7_1","doi-asserted-by":"publisher","DOI":"10.1016\/j.gde.2013.05.005"},{"key":"e_1_2_7_8_1","doi-asserted-by":"publisher","DOI":"10.1523\/JNEUROSCI.19-12-04907.1999"},{"key":"e_1_2_7_9_1","doi-asserted-by":"publisher","DOI":"10.1016\/j.spen.2009.07.003"},{"key":"e_1_2_7_10_1","doi-asserted-by":"publisher","DOI":"10.1093\/brain\/awt358"},{"key":"e_1_2_7_11_1","doi-asserted-by":"publisher","DOI":"10.1038\/386796a0"},{"key":"e_1_2_7_12_1","doi-asserted-by":"publisher","DOI":"10.1093\/cercor\/bhs395"},{"key":"e_1_2_7_13_1","doi-asserted-by":"publisher","DOI":"10.1038\/nature06514"},{"key":"e_1_2_7_14_1","doi-asserted-by":"crossref","first-page":"184","DOI":"10.1016\/j.ydbio.2004.09.019","article-title":"The axon guidance defect of the telencephalic commissures of the JSAP1\u2010deficient brain was partially rescued by the transgenic expression of JIP1","volume":"227","author":"Ha H.Y.","year":"2005","journal-title":"Dev. 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