Targeted inactivation of Hoxb8 affects survival of a spinal ganglion and causes aberrant limb reflexes
| Autor: | Jeroen Korving, Jacqueline Deschamps, Mark Reijnen, Eric van den Akker, Antje Brouwer, Frits Meijlink |
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| Rok vydání: | 1999 |
| Předmět: |
Genetically modified mouse
Male Embryology Recombinant Fusion Proteins Mutant Mice Inbred Strains Biology Exon Mice Ganglia Spinal medicine Animals Gene Silencing Body Patterning Homeodomain Proteins Movement Disorders Reflex Abnormal HOXB8 Gene Expression Regulation Developmental Extremities Anatomy Exons beta-Galactosidase Mice Mutant Strains Spine Cell biology Ganglion Mice Inbred C57BL medicine.anatomical_structure Reflex Female Forelimb Vertebral column Developmental Biology |
| Zdroj: | Mechanisms of development. 89(1-2) |
| ISSN: | 0925-4773 |
| Popis: | Hoxb8 mutant mice were generated by inserting the lacZ coding sequence in frame with the first exon of Hoxb8. These mice express a fusion protein with a functional β-galactosidase activity instead of Hoxb8. Mutant embryos were analyzed for anatomical changes. The results indicate that Hoxb8 is not an indispensable regulator of A-P patterning in the forelimb, unlike suggested by our Hoxb8 gain of function experiments (Charite J, DeGraaff W, Shen S, Deschamps J. Cell 1994;78:589–601). The null mutant phenotypic traits include degeneration of the second spinal ganglion (C2), an abnormality opposite to the alteration in the gain of function transgenic mice. Subtle changes in the thoracic part of the vertebral column were observed as well. Adult homozygous mutants exhibit an abnormal clasping reflex of the limbs. |
| Databáze: | OpenAIRE |
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