1: J Neurosci. 2002 Oct 1;22(19):8523-31. 

Disruption of early events in thalamocortical tract formation in mice lacking
the transcription factors Pax6 or Foxg1.

Pratt T, Quinn JC, Simpson TI, West JD, Mason JO, Price DJ.

Biomedical Sciences, University of Edinburgh, Edinburgh EH8 9XD, United Kingdom.

Early events in the formation of the thalamocortical tract remain poorly
understood. Recent work has suggested that thalamocortical axons follow a path
pioneered by transient thalamic afferents originating from the medial part of
the ventral telencephalon. We studied the development of these transient
afferents and the thalamocortical tract in mutant mice lacking transcription
factors normally expressed in the dorsal thalamus or ventral telencephalon. Pax6
is expressed in the dorsal thalamus, but not in the medial part of the ventral
telencephalon, and the thalamocortical tract fails to form in Pax6(-/-) embryos.
We found that transient thalamic afferents from the ventral telencephalon do not
form in Pax6(-/-) embryos; this may contribute to the failure of their
thalamocortical development. The distribution of Pax6(-/-) cells in
Pax6(-/-)<--> Pax6(+/+) chimeras supports conclusions drawn from forebrain
marker gene expression that Pax6 is not required for the normal development of
the medial part of the ventral telencephalon but is required in the dorsal
thalamus. Failure of the transient afferent pathway to develop is therefore
likely a cell nonautonomous defect reflecting primary defects in the thalamus.
We then examined the formation of thalamic afferents and efferents in Foxg1(-/-)
embryos, which lack recognizable ventral telencephalic structures. In these
embryos thalamic efferents navigate correctly through the thalamus but fail to
turn laterally into the telencephalon, whereas other axons are able to cross the
diencephalic/telencephalic boundary. Our results support a role for the ventral
telencephalon in guiding the early development of the thalamocortical tract and
identify a new role for the transcription factor Pax6 in regulating the ability
of the thalamus to attract ventral telencephalic afferents.

PMID: 12351726 [PubMed - indexed for MEDLINE]


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2: Dev Biol. 1999 Jul 1;211(1):53-63. 

Dorsal-ventral patterning defects in the eye of BF-1-deficient mice associated
with a restricted loss of shh expression.

Huh S, Hatini V, Marcus RC, Li SC, Lai E.

Cell Biology Program, Memorial Sloan-Kettering Cancer Center, New York, New
York, 10021, USA.

Brain factor 1 (BF-1) is a winged-helix transcription factor with restricted
expression in the anterior optic vesicle and in the telencephalic
neuroepithelium of the neural tube. We have previously found that targeted
disruption of the BF-1 gene results in hypoplasia of the cerebral hemispheres,
which is more severe in structures derived from the ventral telencephalon. Here
we show that the loss of BF-1 leads to multiple developmental anomalies of the
eyes. The most ventral structure arising from the optic vesicle, the optic
stalk, is missing and is replaced by an expanded retina. Ventral closure of the
optic cup and choroid fissure does not occur. These dorsal-ventral patterning
defects are not limited to the BF-1-expressing (anterior) cells, but also
involve the cells of the posterior optic vesicle. Sonic hedgehog (shh)
expression within the ventral telencephalic neuroepithelium is specifically lost
in the BF-1(-/-) mutant. Taken together, these findings suggest that shh
produced at this site plays a role in patterning the developing eye. This
localized deficit in shh expression may also contribute to the prominence of the
ventral defects in the telencephalon of the BF-1(-/-) mutant. Copyright 1999
Academic Press.

PMID: 10373304 [PubMed - indexed for MEDLINE]


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