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. Author manuscript; available in PMC: 2015 May 12.
Published in final edited form as: Development. 2007 Nov;134(22):4095–4106. doi: 10.1242/dev.010272

Fig. 1. Loss or gain of Lrp6 function inhibits convergent extension without affecting tissue patterning.

Fig. 1

(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 β-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 β-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 β-catenin DNA (100 pg). Convergent-extension defects due to Lrp6MO injections are rescued by co-injecting lrp6FL mRNA, but not β-catenin DNA. Anteriorized embryos had an average dorsoanterior index (DAI) of 8 (Kao and Elinson, 1988). β-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).