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Local changes in BMP signaling alter rib morphology.AâC. Alcian-blue stained rib cages from E14.5 control animals (A), and embryos expressing either a constitutively active (Ex4r-caBmprIb) (B) or dominant negative (Ex4r-dnBmprIb) (C) form of BmprIb under the control of the Ex4r sequence. Increased BMP signaling in the lateral rib perichondrium triggers local rib overgrowth (arrow, B). Decreased BMP signaling alters dorsoventral rib trajectory (bracket, C). DâF. Coronal rib cryosections from Ex4r-caBmprIb and Ex4r-dnBmprIb transgenic embryos also expressing Ex4r-lacZ. Dashed lines denote rib boundaries. D. Normal rib morphology in control embryo. E. The lateral perichondrium forms excess cartilage in Ex4r-caBmprIb embryos. F. Decreased BMP signaling in Ex4r-dnBmprIb embryos does not affect rib cross-sectional shape. The turtle gene products act as netrin-independent midline attractants. (A) Df(1)NP-5 homozygous embryos are missing the netA and netB genes and, consequently, exhibit gaps in their longitudinal connectives (arrow) and fragmented commissures (arrowhead), as revealed by BP102 staining. (B, C) Df(1)NP-5; tutlex383/+ embryos show an enhancement of both defects (B, arrow and arrowhead), while Df(1)NP-5; tutlex383 double mutants have an extreme reduction in commissures, with only one thin fragmented commissure formed throughout the length of the embryo (C). (D) fraGA957 homozygous embryos exhibit gaps in their longitudinal connectives (arrow) and fragmented commissures (arrowhead) as revealed by BP102 staining. (E)fraGA957, tutlex383/+ embryos show an enhancement of both defects. while fraGA957,tutlex383 double mutants have an extreme reduction in commissures (arrowhead) (G) slit1/+, robo5/+ embryos have a reduction in slit signaling that can produce a minor midline crossing defect revealed by FasII staining (arrowhead). (H, I) slit1/+, robo5/+, tutlex383/+ triple heterozygotes do not show any enhancement nor suppression of the FasII axon crossing defect compared to slit1/+, robo5/+ double heterozygotes alone. (J) abl1 homozygous embryos do not show any defect in commissure or longitudinal connectives as revealed by BP102 staining (arrow and arrowhead). (K, L) tutlex383; abl1/+ embryos show an enhancement of commissural defects (K), while tutlex383; abl1 double mutants have an extreme reduction in commissure formation (L, arrow) and fragmented longitudinal connectives (L, arrowhead).
Lister Hill National Center for Biomedical Communications
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