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Fig. 5. The absence of LIFRß signaling during development results in the
precocious differentiation of E12.5 VZ precursors in the lateral ganglionic
eminence (LGE). The number of GSH2+ cells within the LGE VZ was significantly
decreased in the Lifr-/- embryos (A; 911±23)
relative to Lifr+/+/Lifr+/-
littermates (B; 1324±44; paired t-test
**P=0.0006; n=4). By contrast, the number of
MASH1+ cells was significantly increased in the Lifr-/-
embryos (C; 802±30) relative to littermate controls (D; 504±22;
paired t-test **P=0.0007; n=3).
Double-labeling with GSH2 and MASH1 revealed more GSH2-MASH1+ precursors in
the VZ of the Lifr-/- littermates (E,F). Increased DLX2
expression was observed within the VZ of Lifr-/- embryos
(G,H). Double-labeling with MASH1 and DLX2 revealed an increase in the
population of MASH1+DLX2+ cells (P4 precursors) in the VZ of
Lifr-/- embryos (I,J). DLX1 expression was increased
within the VZ of Lifr-/- (L) compared with
Lifr+/+/Lifr+/- embryos (K). GAD65
expression was restricted to the SVZ and mantle zone regions in wild-type
embryos (M), but ectopically expressed within the VZ of
Lifr-/- embryos (N; arrows indicate GAD65 staining). The
number of surface pHH3+ cells (VZ precursors) was reduced by 40% in the LGE of
the Lifr-/- embryos compared with littermate
Lifr+/+/Lifr+/- embryos (O,P; paired
t-test **P=0.0005; n=4). The number of
non-surface pHH3+ cells (SVZ precursors) was not significantly different
between the Lifr-/- and
Lifr+/+/Lifr+/- littermates. For all
experiments, n
3. Scale bars: in A, 100 µm for A-D,G,H,K-N; in
E, 50 µm for E,F,I,J; in M, 100 µm for M-P.
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