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1.
Figure 4.

Figure 4. From: GLUT10 is required for the development of the cardiovascular system and the notochord and connects mitochondrial function to TGF? signaling.

Tgfbr1 inhibitor (LY-364947) treatment. (A) Wild-type fish treated with 0 and 40 µm LY-364947. Blood pooling in the sinus venosus is indicated by a black arrow. (B) Fli1:eGFP fish treated with 0 or 40 µm LY-364947. Condensation of the caudal vein plexus is marked by a white arrow. (C) Splice—MO-injected embryo treated with 40 µm LY-364947.

Andy Willaert, et al. Hum Mol Genet. 2012 March 15;21(6):1248-1259.
2.
Figure 5.

Figure 5. From: GLUT10 is required for the development of the cardiovascular system and the notochord and connects mitochondrial function to TGF? signaling.

Transcriptome analysis in slc2a10 knockdown and tgfbr1 (LY-364947) inhibitor-treated zebrafish. (A) Venn diagram depicting the overlap between differentially expressed gene transcripts (≥1.5-fold expression; P< 0.05) after LY-364947 treatment and after splice—MO injection. (B) The correlation between gene transcripts with transcript-level changes of ≥1.5-fold (P< 0.05) after splice—MO injection and after LY-364947 treatment (Pearson correlation).

Andy Willaert, et al. Hum Mol Genet. 2012 March 15;21(6):1248-1259.
3.
Figure 6.

Figure 6. From: GLUT10 is required for the development of the cardiovascular system and the notochord and connects mitochondrial function to TGF? signaling.

Knockdown of slc2a10 does not affect mitochondrial morphology but decreases the OCR. Electron micrographs of mitochondria from control—MO-injected (A) and slc2a10—MO-injected (B) embryos at 52 hpf show normal morphology. Magnification bars: 500 nm. The measurement of OCR of control—MO and slc2a10—MO-injected embryos at 3–11 hpf (C) and at 20–28 hpf (D). FCCP, an uncoupler, and rotenone (a complex I inhibitor) were added at the indicated time points.

Andy Willaert, et al. Hum Mol Genet. 2012 March 15;21(6):1248-1259.
4.
Figure 2.

Figure 2. From: GLUT10 is required for the development of the cardiovascular system and the notochord and connects mitochondrial function to TGF? signaling.

Slc2a10 knockdown phenotype. (A) General morphology of slc2a10 morphants at 48 hpf. Besides wild-type embryos, three different embryo classes can be discerned based on general notochord/tail structure. (B) Class 1 and 2 morphants exhibit bowing and kinking of the notochord (arrowheads). (C) Confocal microscopy in Fli1:eGFP zebrafish injected with slc2a10 splice—MO. In Class 1 and 2 embryos, the vasculature is incomplete and shows irregular patterning, especially of the caudal vein plexus. (D) Blood pooling in the sinus venosus of the heart (black arrows). DA, dorsal aorta; Se, segmental vessels; CA, caudal artery; CVP, caudal vein plexus.

Andy Willaert, et al. Hum Mol Genet. 2012 March 15;21(6):1248-1259.
5.
Figure 3.

Figure 3. From: GLUT10 is required for the development of the cardiovascular system and the notochord and connects mitochondrial function to TGF? signaling.

MO knockdown of slc2a10. (A) Schematic representation of slc2a10 splicing after splice—MO injection. A black bar represents the target position of the splice—MO. Arrows denote the position of the RT–PCR primers in exons 1 and 3. (B) Agarose gel electrophoresis of slc2a10 RT–PCR samples (from control- and splice—MO-injected embryos). In control—MO-injected embryos, a 1300 bp product corresponds to the full-length slc2a10 mRNA. In splice—MO-injected embryos, a 117 bp fragment represents skipping of exon 2. (C) Quantitative PCR analysis shows a 50% reduction in slc2a10 expression in splice—MO-injected compared with control—MO-injected embryos. *P< 0.05 (95% confidence intervals of the means do not overlap).

Andy Willaert, et al. Hum Mol Genet. 2012 March 15;21(6):1248-1259.
6.
Figure 1.

Figure 1. From: GLUT10 is required for the development of the cardiovascular system and the notochord and connects mitochondrial function to TGF? signaling.

Evolutionary conservation of the SLC2A10 gene and GLUT10 protein. (A) The structure of the human SLC2A10 and the zebrafish slc2a10 genes with coding (full boxes) and untranslated (empty boxes) regions shown. MO target regions 1 and 2 are depicted underneath the slc2a10 gene structure. (B) Multiple amino acid sequence alignment of GLUT10 among different species (Clustal W2) (46). Predicted TMDs for human GLUT10 are marked by black bars (47). Boxes indicate sequence motifs, conserved in vertebrate glucose transporters or class 3 sugar transporter facilitators, which are also conserved for GLUT10 among different species including zebrafish (47,48). The N341LTL glycosylation motif in glut10 is underlined. Conservation of amino acid sequences are shown below the alignment: ‘*’ means residues identical in all sequences in the alignment; ‘:’ means conserved substitutions; ‘.’ means semi—conserved substitutions; space means no conservation. Hs, human; Bt, cow; Mm, mouse; Rn, rat; Gg, chicken; Xt, frog; Dr, zebrafish.

Andy Willaert, et al. Hum Mol Genet. 2012 March 15;21(6):1248-1259.
7.
Figure 7.

Figure 7. From: GLUT10 is required for the development of the cardiovascular system and the notochord and connects mitochondrial function to TGF? signaling.

Knockdown of slc2a10 downregulates TGFβ-like transcriptional responses and rescues smad7 morphant phenotypes. (A) A p3TP-lux TGFβ-responsive reporter construct was injected in the presence or in the absence slc2a10—MO. Luciferase activity was assayed at 24 hpf from embryo lysates and compared with uninjected embryos. Pairwise comparison of experimental groups was performed using Student's t-test with P-values shown on the right. RLU, relative light units. (B) Partial rescue of smad7 morphants by simultaneous administration of slc2a10—MO as viewed at 48 hpf. Administration of 1 ng smad7—MO causes severely shortened tail, underdeveloped mesodermal tissues, small head and pericardiac edema. Injection of 7.5 ng of slc2a10—MO caused milder shortening and bending of the embryo and pericardiac edema. The combination of 1 ng smad7 and 7.5 ng slc2a10—MO showed a marked improvement in the tail length, head size and heart morphology relative to smad7—MO treatment only. (C) The heart rate of smad7 morphants was severely reduced compared with control—MO- injected embryos. A smaller decrease was observed in response to slc2a10—MO, combined treatment of embryos with slc2a10- and smad7—MO improved the heart rate relative to smad7—MO only.

Andy Willaert, et al. Hum Mol Genet. 2012 March 15;21(6):1248-1259.

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