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Loss of Hox-A1 (Hox-1.6) function results in the reorganization of the murine hindbrain

Carpenter, Ellen M., Goddard, Judy M., Chisaka, Osamu, Manley, Nancy R., Capecchi, Mario R.·1993·Development

Abstract

Targeted disruption of the murine hox-A1 gene results in severe defects in the formation of the hindbrain and associated cranial ganglia and nerves. Carbocyanine dye injections were used to trace afferent and efferent projections to and from the hindbrain in hox-A1 /hox-A1 mutant mice. Defects were observed in the position of efferent neurons in the hindbrain and in their projection patterns. In situ hybridization was used to analyze the transcription pattern of genes expressed within specific rhombomeres. Krox-20, int-2 (fgf-3), and hox-B1 all display aberrant patterns of expression in hox-A1 mutant embryos. The observed morphological and molecular defects suggest that there are changes in the formation of the hindbrain extending from rhombomere 3 through rhombomere 8 including the absence of rhom-bomere 5. Also, motor neurons identified by their axon projection patterns which would normally be present in the missing rhombomere appear to be respecified to or migrate into adjacent rhombomeres, suggesting a role for hox-A1 in the specification of cell identity and/or cell migration in the hindbrain.

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Research works printed but not linked: 27

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Cited by

Metadata

Authors
Carpenter, E. M., Goddard, J. M., Chisaka, O., Manley, N. R., & Capecchi, M. R.
Venue
Development
Published
1993-08-01
Volume
118
Issue
4
Pages
1063-1075
ISSN
  • 0950-1991 (ISSN-L)
  • 1477-9129
OpenAlex
W2125246072
Cited by
345
References
0
FWCI
8.37
Type
journal article
Language
en
Open access
closed

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