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Fig. 3. Phenotypes of mice carrying epidermal-specific deletions of
Bmpr1a. (A) K14-Cre43; Bmpr1acl/cl
(right) and K14-Cre43; Bmpr1acl/+ control (left)
newborns. The homozygous mutant lacks hindlimbs (blue arrow) and has open eyes
(black arrow). (B) Ventral view of P13 bcre-32;
Bmpr1acl/null (right) and bcre-32;
Bmpr1acl/+ (left) littermates. The mutant lacks
mid-ventral hair (arrow). (C) P20 K14-Cre52; Bmpr1acl/cl
(right) and K14-Cre52; Bmpr1acl/+ (left)
littermates. (D,E) Absence of incisor teeth (arrows) in a K14-Cre52;
Bmpr1acl/cl mouse at P20 (E), compared with a heterozygous
littermate control (D). (F) K14-Cre40;
Bmpr1acl/cl (right) and K14-Cre40;
Bmpr1acl/+ (left) littermates at P34. (G)
K14-Cre40; Bmpr1acl/cl mouse at P34. (H)
K14-Cre40; Bmpr1acl/cl mouse at 5 months. Arrows
indicate pigment accumulations. (I) Uninduced
K14-Cre-ERT2; Bmpr1acl/cl mouse at 5
months. (J) Front paws from uninduced 5-month-old
K14-Cre-ERT2; Bmpr1acl/cl mouse
showing growths under the nails (arrows). (K,L) Anti-BMPR1A immunofluorescence
(red) of newborn K14-Cre43; Bmpr1acl/+ control
(K) and K14-Cre43; Bmpr1acl/cl (L) skin
cryosections. BMPR1A is present in control epidermis and hair follicle (HF),
but only background basal lamina staining is detected in mutant skin. Nuclei
are counterstained with Hoechst 33258. (M) Left side: PCR amplification of
genomic DNA from epidermis, and dermis containing HF germs, from a newborn
K14-Cre43; Bmpr1acl/cl mouse and a
Bmprcl/+ littermate control. Primers detect the
unrecombined floxed (FL), wild-type (WT) and recombined (lacking exon 2;
X) alleles, and produce amplification products of 230 bp, 150 bp and
180 bp, respectively. Right side: PCR amplification of genomic DNA from organs
of a 5-month-old uninduced K14-Cre-ERT2;
Bmpr1acl/cl mouse using the same primers.
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