The transcription factors Nkx2.2 and Nkx2.9 play a novel role in floor plate development and commissural axon guidance

• DOI: 10.1242/dev.053819
• Publication Date: 2010-11-11T01:43:48Z
• Authors: Andreas Holz; Heike Kollmus; Jesper Ryge; Vera Niederkofler; Jose Dias; Johan Ericson; Esther T. Stoeckli; Ole Kiehn; Hans-Henning Arnold
• Keywords: Floor plate; Commissure; OLIG2; Progenitor; Transcription

The transcription factors Nkx2.2 and Nkx2.9 have been proposed to execute partially overlapping functions in neuronal patterning of the ventral spinal cord response graded sonic hedgehog signaling. present report shows that mice lacking both Nkx2 proteins, presumptive progenitor cells p3 domain neural tube convert motor neurons (MN) never acquire fate V3 interneurons. This result supports concept are required establish by repressing early MN lineage-specific program, including genes like Olig2. proteins also perform an additional, hitherto unknown, function development non-neuronal floor plate cells. Here, we demonstrate loss results anatomically smaller functionally impaired causing severe defects axonal pathfinding commissural neurons. Defective plates were seen Nkx2.2(+/-);Nkx2.9(-/-) compound mutants even single Nkx2.9(-/-) mutants, suggesting is sensitive dose and/or timing expression. Interestingly, adult compound-mutant exhibit abnormal locomotion, a permanent or intermittent hopping gait. Drug-induced locomotor-like activity cords mutant neonates affected, demonstrating increased variability left-right flexor-extensor coordination. Our data argue contribute crucially formation networks as central pattern generators for locomotor cord. As affect development, control axon trajectories might be underlying mechanism.