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Hox transcription factors influence motoneuron identity through the integrated actions of both homeodomain and non‐homeodomain regions
Author(s) -
Misra Mala,
Sours Emily,
LanceJones Cynthia
Publication year - 2012
Publication title -
developmental dynamics
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.634
H-Index - 141
eISSN - 1097-0177
pISSN - 1058-8388
DOI - 10.1002/dvdy.23763
Subject(s) - homeobox , biology , hox gene , emx2 , transcription factor , morphogen , spinal cord , genetics , microbiology and biotechnology , anatomy , neuroscience , gene
Abstract Background : Hox transcription factors play a critical role in the specification of motoneuron subtypes within the spinal cord. Our previous work showed that two orthologous members of this family, Hoxd10 and Hoxd11, exert opposing effects on motoneuron development in the lumbosacral (LS) spinal cord of the embryonic chick: Hoxd10 promotes the development of lateral motoneuron subtypes that project to dorsal limb muscles, while Hoxd11 represses the development of lateral subtypes in favor of medial subtypes that innervate ventral limb muscles and axial muscles. The striking degree of homology between the DNA‐binding homeodomains of Hoxd10 and Hoxd11 suggested that non‐homeodomain regions mediate their divergent effects. In the present study, we investigate the relative contributions of homeodomain and non‐homeodomain regions of Hoxd10 and Hoxd11 to motoneuron specification. Results : Using in ovo electroporation to express chimeric and mutant constructs in LS motoneurons, we find that both the homeodomain and non‐homeodomain regions of Hoxd10 are necessary to specify lateral motoneurons. In contrast, non‐homeodomain regions of Hoxd11 are sufficient to repress lateral motoneuron fates in favor of medial fates. Conclusions : Together, our data demonstrate that even closely related Hox orthologues rely on distinct combinations of homeodomain‐dependent and ‐independent mechanisms to specify motoneuron identity. Developmental Dynamics 241:718–731, 2012. © 2012 Wiley Periodicals, Inc.