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Fig. 1. Loss or gain of Lrp6 function inhibits convergent extension without
affecting tissue patterning. (A) Dorsal injections of Lrp6
morpholino (LRP6MO, 40 ng) or mRNA (1 ng) cause defects in neural and
mesodermal convergent extension. In contrast to uninjected or ß-catenin
(50 pg) injected siblings, embryos with altered Lrp6 levels are not fully
elongated (less than 70% of the length of controls) and have split or thicker
notochords resembling that of Xdd-(2 ng) or Dkk1-(400 pg) injected embryos.
Lrp6 or ß-catenin mRNA levels were chosen so as to cause similar
percentages of anterior duplication when injected ventrally (bar graph). For
each injection, Tor70 antibody staining for notochord is shown in the lower
panels. Scale bars: 0.5 mm. (B) The anteriorizing effect of Lrp6MO
injection (30 ng) is rescued by co-injecting full-length lrp6 mRNA
(LRP6FL, 500 pg) or ß-catenin DNA (100 pg). Convergent-extension defects
due to Lrp6MO injections are rescued by co-injecting lrp6FL mRNA, but
not ß-catenin DNA. Anteriorized embryos had an average dorsoanterior
index (DAI) of 8 (Kao and Elinson,
1988). ß-catenin DNA injection resulted in posteriorized
embryos (60% affected, 72 embryos injected) having an average DAI of 2. Error
bars indicate standard deviation. Numbers of embryos scored are indicated in
parentheses. (C) Mesendodermal [Bra (Xbra), Chordin, Goosecoid (Gsc),
Sizzled, Endodermin (Endd)] and ectodermal (Otx2, Xag1, epidermal Keratin)
markers are expressed in developing embryos injected with lrp6 mRNA
(1 ng), dkk1 mRNA (200 pg) or Lrp6MO (40 ng), indicating that the
effect of Lrp6 on convergent extension is not due to altered tissue
patterning. Loading control: ODC (ornithine decarboxylase).
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