Hoxb13 mutations cause overgrowth of caudal spinal cordand tail vertebrae
| Autor: | Kyriakos D. Economides, Lori M. Zeltser, Mario R. Capecchi |
|---|---|
| Rok vydání: | 2003 |
| Předmět: |
Tail
Mesoderm Axial skeleton Mutant Proliferation Apoptosis Biology Hoxb genes Myoblasts Mice Ganglia Spinal medicine Animals Allele Hox gene Gene Molecular Biology Homeodomain Proteins Neural tube Gene Expression Regulation Developmental Cell Biology Spinal cord Molecular biology Phenotype Axons Spine Secondary neurulation medicine.anatomical_structure Spinal Cord Hoxb13 Mutation Developmental Biology |
| Zdroj: | Developmental Biology. 256(2):317-330 |
| ISSN: | 0012-1606 |
| DOI: | 10.1016/s0012-1606(02)00137-9 |
| Popis: | To address the expression and function of Hoxb13, the 5′ most Hox gene in the HoxB cluster, we have generated mice with loss-of-function and β-galactosidase reporter insertion alleles of this gene. Mice homozygous for Hoxb13 loss-of-function mutations show overgrowth in all major structures derived from the tail bud, including the developing secondary neural tube (SNT), the caudal spinal ganglia, and the caudal vertebrae. Using the β-galactosidase reporter allele of Hoxb13, also a loss-of-function allele, we found that the expression patterns of Hoxb13 in the developing spinal cord and caudal mesoderm are closely associated with overgrowth phenotypes in the tails of homozygous mutant animals. These phenotypes can be explained by the observed increased cell proliferation and decreased levels of apoptosis within the tail of homozygous mutant mice. This analysis of Hoxb13 function suggests that this 5′ Hox gene may act as an inhibitor of neuronal cell proliferation, an activator of apoptotic pathways in the SNT, and as a general repressor of growth in the caudal vertebrae. |
| Databáze: | OpenAIRE |
| Externí odkaz: |
|
Full Text from ScienceDirect