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FIGURE 2. Overexpression or knockdown of ets1 causes defects in NC derivatives. A and B, ets1 overexpression (500 pg/embryo; 85%; 23 of 27) caused loss of pigment throughout the body and inhibition of head structures. C–F, knockdown of ets1using ets1MO1 (94%; 30 of 32) or ets1MO2 (94%; 33 of 35) showed similar pigment loss and repression of head. G, categories of defects induced by either 30 ng of ets1MO1 separately or by co-injection (inj.) with 250 pg of ets1 mRNA. Numbers at the top indicate total embryos scored at stage 35 from three independent experiments. H and I, either 60 ng of ets1MO1 or ets1MO2 was injected into two-cell stage embryos, the embryos were collected at stage 11, and Ets1 protein was detected by α-Ets1 antibody. Tubulin was used as an internal control. The bands on Western blots (H) were quantified in I. J–L, the expression of cranial nerve marker gene sncg is disrupted in embryos injected with 250 pg of ets1 mRNA (K; 85%, 28 of 33) or 30 ng of ets1MO1 (L; 72%, 18 of 25). con, control. M–P, either ets1-GR or dnets1-GR mRNA (500 pg/embryo) was injected into two-cell stage embryos. The injected embryos were treated with DEX starting at stage 13. Loss of pigment and inhibition of anterior axis were observed in DEX-treated embryos (N, 81%, 26 of 32; P, 74%, 17 of 23) but not in untreated embryos (M, 4%, 1 of 26; O, 0%, 0 of 11). Likewise, the expression of sncg was much reduced in the embryos injected with either ets1-GR or dnets1-GR and sequentially treated with DEX (R, 84%, 26 of 31; T, 84%, 21 of 25) but remained normal in embryos without DEX treatment (Q, 0%, 0 of 29; S, 0%, 0 of 18). U–W, cranial cartilage formation in control (U) and embryos injected with ets1 mRNA (V; 85%, 51 of 60) or ets1MO (W; 83%, 33 of 40) was examined by Alcian blue staining. An asterisk indicates the injected side. con, control. Image published in: Wang C et al. (2015) Copyright © 2015. Image reproduced with permission of the publisher and the copyright holder. This is an Open Access article distributed under the terms of the Creative Commons Attribution License. Gene Synonyms Species Stage(s) Tissue sncg.S bcsg1, gamma-synuclein, sncg-a, sncg-b X. laevis Throughout NF stage 27 trigeminal placode trigeminal ganglion cement gland primordium Image source: Published Experiment + Assay Source Phenotypes and Disease Xla Wt + ets1 + NF39 (morphology) fig.2.b Anatomical Phenotype decreased pigmentation in the whole organism decreased size of the head Xla Wt + ets1 MO + NF39 (morphology) fig.2.d Anatomical Phenotype abnormally ruffled dorsal fin Xla Wt + ets1 MO + NF39 (morphology) fig.2.d, g Anatomical Phenotype decreased pigmentation in the whole organism decreased size of the head Xla Wt + ets1 MO + NF39 (morphology) fig.2.f Anatomical Phenotype abnormally ruffled dorsal fin decreased pigmentation in the whole organism decreased size of the head Xla Wt + ets1 + NF39 (in situ hybridization) fig.2.k Expression Phenotype decreased amount sncg.L expression in cranial nerve decreased amount sncg.L expression in trigeminal nerve Xla Wt + ets1 MO + NF39 (in situ hybridization) fig.2.l Expression Phenotype decreased amount snca.L expression in cranial nerve decreased amount snca.L expression in trigeminal nerve Xla Wt + ets1-GR + DEX + NF39 (morphology) fig.2.n Anatomical Phenotype decreased pigmentation in the whole organism decreased size of the head Xla Wt + dnets1-GR + DEX + NF39 (morphology) fig.2.p Anatomical Phenotype decreased pigmentation in the whole organism decreased size of the head Xla Wt + ets1 + NF39 (in situ hybridization) fig.2.v Anatomical Phenotype abnormally incomplete structure of head Xla Wt + ets1 MO + NF39 (in situ hybridization) fig.2.w Anatomical Phenotype abnormally incomplete structure of head Larger Image Printer Friendly View

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