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Fig. 1. Hedgehog signaling promotes chondrocyte hypertrophy in the absence of
PTHrP signaling. (A,B) Forelimbs of
PTHrP-/- or wild-type E14.5 embryos cultured for 36 hours
in the presence or absence of recombinant Shh protein or cyclopamine. Treated
limbs were compared with untreated contralateral control ones. Serial sections
of the proximal humerus of the cultured limbs were hybridized with
35S riboprobes of Ihh (A) or Col10a1 (B). The
distances from the articular end to the Ihh/Col10a1 domain
in the untreated wild-type and PTHrP-/- embryos are
indicated by orange lines. This distance was increased in the Shh-treated
wild-type humerus but reduced in the Shh-treated PTHrP-/-
humerus (white lines) compared with the untreated contralateral controls. This
distance was reduced in the cyclopamine-treated wild type, but increased in
the PTHrP-/- humerus (green lines) compared with the
untreated controlateral controls. (C) Statistical analysis (paired
Student's t-test) of the distance from articular chondrocytes to the
hypertrophic zone between treated and untreated contralateral limbs. Numbers
(n) of analyzed limbs are indicated. (D) Serial sections of
E14.5 distal humeri of the indicated genotypes stained with Safranin O (upper
panel) and hybridized with a 35S Col10a1 riboprobe (lower
panel) to detect chondrocyte hypertrophy. The distance from the articular end
to the Col10a1 expression domain (orange lines) in the
PTHrP-/- embryos was reduced compared with that in the
wild-type embryos. This distance in the
PTHrP-/-;UAS-cIhh;Col2a1-Gal4 double mutant was further
reduced compared with that of the PTHrP-/- embryos.
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