Neuroscience 2003 Abstract
| Presentation Number: | 34.22 |
|---|---|
| Abstract Title: | Retinal axon path finding defects in mice lacking the transcription factor FoxG1. |
| Authors: |
Pratt, T.*1
; Simpson, T. I.1
; Tian, N.1
; Price, D. J.1
; Mason, J. O.1
1Genes and Develop. Group, Biomed. Sci., Univ. Edinburgh, Edinburgh, United Kingdom |
| Primary Theme and Topics |
Development - Axonal and Dendritic Development -- Axon growth and guidance: receptors and signaling mechanisms |
| Session: |
34. Axon Growth and Guidance: Receptors and Signaling Mechanisms--Intracellular Signaling Poster |
| Presentation Time: | Saturday, November 8, 2003 2:00 PM-3:00 PM |
| Location: | Morial Convention Center - Hall F-I, Board # B44 |
| Keywords: | optic chiasm, growth cone, optic tract, BF1 |
The transcription factor Foxg1 (BF1) is expressed in the developing eye and brain. Mice lacking Foxg1 exhibit dramatic hypoplasia of the telencephalon and distortions to the eye. Remarkably, in spite of these defects the Foxg1 mutant retina does project axons to the brain . The aim of this study is to establish which features of retinal axon navigation are affected as a result of the absence of Foxg1.
During normal development axons leave the retina and grow over the ventral surface of the hypothalamus towards the midline. At a defined point on the ventral surface of the hypothalamus (the optic chiasm) the axons either cross the midline and grow dorsally towards targets on the opposite side of the brain (crossed or contralateral projection) or do not cross and grow towards targets on the same side of the brain (uncrossed or ipsilateral projection). In rodents the ipsilateral projection is much smaller than the contralateral projection and originates from the ventral temporal part of the retina whereas the contralateral projection originates from all parts of the retina.
Anterograde tract tracing using carbanocyanine dyes DiI and DiA placed in the eyes of Foxg1 mutant embryos shows that axons exit the retina and grow towards the midline. In the wild-type the majority of retinal axons cross the midline at the optic chiasm whereas in the mutant a much higher proportion do not cross the midline. Regardless of this midline crossing error the axons appear to follow a normal trajectory dorsally over the thalamus and towards the midbrain. Retrograde tract tracing shows that the distribution of ipsilaterally projecting cells is altered in the mutant retina.
The Foxg1 mutant phenotype therefore provides a means to dissect the mechanism by which the transcription factor Foxg1 regulates the behaviour of retinal growth cones at the optic chiasm.
During normal development axons leave the retina and grow over the ventral surface of the hypothalamus towards the midline. At a defined point on the ventral surface of the hypothalamus (the optic chiasm) the axons either cross the midline and grow dorsally towards targets on the opposite side of the brain (crossed or contralateral projection) or do not cross and grow towards targets on the same side of the brain (uncrossed or ipsilateral projection). In rodents the ipsilateral projection is much smaller than the contralateral projection and originates from the ventral temporal part of the retina whereas the contralateral projection originates from all parts of the retina.
Anterograde tract tracing using carbanocyanine dyes DiI and DiA placed in the eyes of Foxg1 mutant embryos shows that axons exit the retina and grow towards the midline. In the wild-type the majority of retinal axons cross the midline at the optic chiasm whereas in the mutant a much higher proportion do not cross the midline. Regardless of this midline crossing error the axons appear to follow a normal trajectory dorsally over the thalamus and towards the midbrain. Retrograde tract tracing shows that the distribution of ipsilaterally projecting cells is altered in the mutant retina.
The Foxg1 mutant phenotype therefore provides a means to dissect the mechanism by which the transcription factor Foxg1 regulates the behaviour of retinal growth cones at the optic chiasm.
Supported by Funded by the Medical Research Council and The Wellcome Trust.
Sample Citation:
[Authors]. [Abstract Title]. Program No. XXX.XX. 2003 Neuroscience Meeting Planner. New Orleans, LA: Society for Neuroscience, 2003. Online.
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