About ZFIN
The Zebrafish Information Network (ZFIN) is the database of genetic and genomic data for the zebrafish (Danio rerio) as a model organism. ZFIN provides a wide array of expertly curated, organized and cross-referenced zebrafish research data.
Learn MoreNew Data in ZFIN
Fig. 6 of Savage et al., 2019
tmem33 knockdown reduces endothelial Notch and ERK signalling during angiogenesis. a–c Notch reporter expression is unaffected by injection of 0.4 ng tmem33 morpholinos at 26 hpf. Notch signalling activity in control embryos is present in neural tube (blue arrowhead) and DA (red arrowhead) (c, unpaired t-test; t = 0.5553; DF = 20; 2 repeats; n = 5 or 6 embryos per group). Scale bars 50 µm. d–f Injection of 0.4 ng tmem33 morpholinos reduces Notch reporter expression at 48 hpf. Notch expression in control Tg(csl:venus) embryos is present in the neural tube (blue arrowhead), DA (red arrowhead) and SeAs (white arrowheads) (f, unpaired t-test; p = 0.0451; t = 2.138; DF = 20; 2 repeats; n = 6 and 4 embryos per group). Scale bars 50 µm. g Expression of notch1b, dll4, hey2 and her12 are not significantly altered by tmem33 CRISPRi at 26 hpf (one-way ANOVA using post hoc Tukey’s comparison test. n = 3 repeats). h Expression of notch1b, dll4, hey2 and her12 are significantly reduced at 48 hpf by tmem33 CRISPRi (one-way ANOVA using post hoc Tukey’s comparison test. *p = < 0.05; **p = < 0.01. n = 3 repeats). i–p In comparison with control morphants (i–l), embryos injected with 0.4 ng tmem33 morpholino (m–p) display reduced expression of notch1b within the DA (i, m, red arrowheads) and SeAs (i, m, white arrowheads), dll4 within SeAs (j, n, white arrowheads), hey2 within the DA (k, o, red arrowheads) and her12 within the DA (l, p, red arrowheads) and SeAs (l, p, white arrowheads). Scale bars 100 µm. q–t tmem33 knockdown by CRISPRi reduces endothelial ERK phosphorylation (q, r, SeAs highlighted by yellow outline and white arrowheads). Intensity plot of ERK staining is shown (s, t, SeAs highlighted by yellow outline and white arrowheads). Scale bars 50 µm. u tmem33 crispants display significantly reduced levels of pERK phosphorylation. Pixel intensity normalised to neural tube ERK fluorescence (unpaired t-test, **p = 0.0097, t = 2.993 DF = 14. n = 2 repeats, 4 embryos per group). Source data are provided as a Source Data file
Fig. 4 of Sahu et al., 2019
Reduced tyrosine hydroxylase immunoreactivity in both the morphants and mutants at 5 dpf. (A) (a–d) TH1 immunohistochemistry revealed a loss of the neuronal population in the diencephalic cluster (5,6,11 cell group) in the Ntrk2b and Ntrk2a morphant. The neuronal cell group affected has been encircled. (A) (a′–d′): Higher magnification images of the affected TH cell group. (B) Total cell counts in the diencephalic region of the morphants. (C) The mutants have reduced TH positive cells in the same cell group and could be rescued by mRNA overexpression. (C) (a′–d′) Higher magnification images of the affected TH cell group. (D) TH cell counts from the mutants in the 5,6,11 cell group. (Bars represent Mean ± SEM, one-way ANOVA, Kruskal-Wallis test **p-value < 0.008, ****p-value < 0.0002, Scale bar = 100 um).
Fig. 7 of Villani et al., 2019
Gastrosomal Defects Affect Microglial Functionality (A) 4 dpf wild-type Tg(mpeg:GFP-caax) microglia stained with Nile Blue (cyan) in an embryo treated with Camptothecin to increase apoptosis. Scale bar, 5 μm. The white dotted line marks the gastrosome. (B) SPIM time-lapse of representative 4 dpf wild-type Tg(mpeg:GFP-caax) microglia stained with Nile Blue (cyan) in an embryo treated with Camptothecin to increase apoptosis. Scale bar, 10 μm. The white dotted line marks the shrinking gastrosome. See also Video S8. (C) Quantification of microglia responding to an injury in wild-type and blbNY007 microglia at different developmental stages; wt, 3.5 dpf, n = 20; blbNY007, 3.5 dpf, n = 20; wt, 4 dpf, n = 20; and blbNY007, 4 dpf, n = 16; whiskers: 5th/95th percentile, p value blb embryo). (D) Quantification of engulfment duration in wild-type (n = 20) and blbNY007 microglia (n = 11), whiskers: 5th/95th percentile, p value (E) RAW264.7 macrophages unfed (left column) or fed with HK H2B mCherry cells and fixed 24 h after apoptosis induction (right column). Slc37a2 antibody staining in untreated controls (upper panels) and in cells transfected with an siRNA targeting Slc37a2. (F) Quantification of the gastrosomal size (μm) in RAW macrophages fed with apoptotic HeLa cells in the absence or in the presence of Slc37a2 siRNA, p value < 0.0001. Representative images of this experiment in Figure S3A (yellow arrowheads).
Fig. 4 of Zhang et al., 2019
Defective tooth phenotypes in clcn7-deficient zebrafish. (A) Alcian blue and alizarin red staining results of 5thceratobranchial arch and teeth in control and clcn7 morphants at 5dpf. The malformed teeth were fewer with weak red staining clcn7 morphants. (B) Quantitative comparison of the extent of calcification among WT embryos, control and clcn7 morphants. (C) Comparison of embryonic tooth number. WT and control embryos had 3V1, 4V1 and 5V1 teeth, while clcn7 morphants showed 3V1, 4V1 and 5V1 fewer teeth. (D) Ultrastructure of tooth 4V1 in control and clcn7morphants. clcn7 morphants had malformed tooth and enameloid dysplasia. Red arrows point to the pits on the enameloid surface. For A, B, D: WT n=50, Control MO n=50, clcn7 MO n=50. The white square in the first image of figure A is the region for measuring calcified content in panel B. Error bar represents the SD. The experiment was repeated thrice with the same conditions. The data in image C was one of the representative experimental results. WT n=300, Control MO n=320, clcn7 MO n=300. ** p<0.01, *** p<0.001. Scale bars: 100 μm.
Fig. 4 of Kumar et al., 2019
WISH distribution analysis of zic3 in peli1bknockdown embryos at 14 hpf. Lateral view of zebrafishembryos (A–C). Anterior view (D–F). Posterior view (G–I). WT embryos (A, D, & G), 5′ mismatch controls (B, E, & H), and peli1b morphants injected with 10 ng morpholino at the 1-cell stage (C, F, & I). Red arrowheads show zic3expression and intensity in WT, 5′ mismatch, and peli1bmorphants. (n = 3). Abbreviations: pd- posterior diencephalon, dsc- dorsal spinal cord, dnp- dorsal neural plate, hb- hindbrain, mb- midbrain, dpnp-dorsal posterior neural plate, sp-segmental plate. Scale bar- 50 μm. (For interpretation of the references to color in this figure legend, the reader is referred to the web version of this article.)
Fig. 3 of Zhang et al., 2019
Craniofacial bone and cartilage abnormalities in clcn7 morphants. (A) Craniofacial phenotype comparison between control and clcn7 morphants. Cranial cartilages (blue) and mineralized bones (red) were stained with alcian blue and alizarin red in control and clcn7 morphants at 5 dpf, respectively. (A-C) Compared to WT and Control embryos, clcn7 morphants showed more malformed craniofacial skeletons, and clcn7 mRNA rescued the abnormalities in craniofacial region. (D, E) Abnormal ceratohyal (Ch) angle and altered location of otolith in clcn7 morphants. (F)Quantitative analysis of a series of changes of phenotypic indexes. clcn7 morphants showed obvious changes in the pattern of craniofacial structure. (G) WISH analysis showed the abolished expression of sp7 and col10a1 in cranial skeleton, most notably in the parasphenoid (Ps) and opercle (Op) bones in clcn7 morphants at 3 dpf. (H) Q-PCR analysis confirmed the reduced level of sp7 and col10a1. For A-E, WT n=300, Control MO n=320, clcn7 MO n=300, clcn7 MO + mRNA n=182. For H: Control MO n=50, clcn7 MO n=50. The red arrow indicates abnormal Ch angle, and the white arrow points to abnormal otolith. Ch: ceratohyal. M: Meckel's. Op: opercle. Pq: palatoquadrate. Ps: parasphenoid. WT: wide type. Error bar represents the SD. The experiment was repeated at least thrice with the same conditions. * p<0.05, ** p<0.01, *** p<0.001. Scale bars: 100 μm.
Fig. 3 of Villani et al., 2019
Cloning and Characterization of Slc37a2, the Gene Underlying the blb Phenotype (A) Schematic of the slc37a2 locus. Sequences of the NY007/t30301 allele (C/T mutation) and NA150/t30913 allele (T/A mutation). (B) Dorsal view of a 4 dpf Slc37a2 knockout generated with CRISPR-Cas9 as shown in (A). Scale bar, 30 μm. (C) Dorsal view of a representative immunostaining of a 4 dpf embryo where microglia are in green Tg(mpeg:GFP-caax) and Slc37a2 in red. Scale bar, 30 μm. (D) Magnification of (C). Scale bar, 15 μm. The yellow arrow points to a phagosome positive for Slc37a2. (E) Western blot analysis of Slc37a2 (55 kDa) and Tubulin (48 kDa) in wild-type, blbNY007, and blbNI150. (F) Immunostainings of Slc37a2 (cyan) and Lamp1 (red) in RAW264.7. Scale bar, 5 μm. (G and H) Mass-spectrometry data showing normalized intensities of glucose 6-phosphate (G) not significant, and D-gluconate-6-phosphate (H) significant, p value < 0.0001, in blbNY007 and wild-type.
Fig. 5 of Cal et al., 2019
Detailed visualization of ventral pigment cells in WT and asip1 mutants. (A) Ventral view of 210 dpf WT belly. (B) Belly of 210 dpf WT fish carrying Tg(Kita:GalTA4;UAS:mCherry) (labels melanophores) transgene shows no melanophores in ventral skin. (C) Ventral view of 210 dpf asip1K.O. belly. (D) Belly of 210 dpf asip1K.O. fish carrying Tg(Kita:GalTA4;UAS:mCherry) transgene shows high number of melanophores in ventral skin. (E) Internal view of 210 dpf WT abdominal wall shows a white sheet of iridophores with few internal melanophores (black arrow). (F) Abdominal wall of 210 dpf WT fish carrying Tg(TDL358:GFP) (labels iridophores and glia) transgene displays a uniform and continuous sheet of iridophores. (G) Internal view of 210 dpf asip1K.O. abdominal wall shows a disrupted and discontinuous sheet of iridophores with high number of melanophores (black arrow) and some xanthophores (orange arrow). (H) Abdominal wall of 210 dpf asip1K.O. fish carrying Tg(TDL358:GFP)transgene exhibits a broken sheet of iridophores. Scale bars: 100 μm.
Fig. 6 of Huo et al., 2019
Expression of cancer angiogenesis genes in TANs and effects of neutrophil depletion on liver tumorigenesis and angiogenesis. (A) Heatmap representation of expression of cancer angiogenesis genes extracted from DEGs of TANs. The color codes represent fold changes of expression of each gene in each sample relative to the mean expression of all samples. The list of cancer angiogenesis genes was obtained based on IPA knowledge datbase. (B) Representative confocal images of 6-dpf lyz+ larvae injected with different morpholinos: MO_SC (left, n = 18) or MO_gcsfr (right, n = 20). (C) Numbers of neutrophils in the middle body after injection of morpholinos. Neutrophils were counted in the the middle body surrounding the liver region (from the posterior edge of eye to posterior edge of swimbladder). (D) Representative 3D confocal images of 6-dpf kras−/fli+ and kras+/fli+ larvae injected with MO_SC or MO_gcsfr. For fli+ larvae, both Tg(fli1a::GFP) (left) and Tg(fli1a::RFP) (middle and right) were used. Kras- larvae were LiPan strain (left) with DsRed expression in the liver. (C and D) Quantification of blood vessel density in the liver area (E) and liver size (F) after morpholino injection. N >20 in each group. Statistical significance: *p < 0.05.
Fig. 2 of Han et al., 2019
Vitamin D Signaling Enhances Organismal Size (A) MIP images and quantification of H3P staining of 3 dpf embryos. hpt, hours post-treatment; H3P, phospho-Histone H3. Mean ± SD, Mann-Whitney test and Student's t test. ∗∗∗∗p < 0.0001. n = 11–13. Scale bar, 500 μm. (B) Example and quantification of 4 dpf zebrafish growth. Mean ± SD, Mann-Whitney test and Student’s t test. ∗∗p < 0.01; ∗∗∗p < 0.001. n = 12-14. Scale bar, 500 μm. (C) Growth and rescue of 2 mpf juvenile wild-type (WT) and ubb:cyp24a1 zebrafish. Scale bar, 4 mm. (D) Quantification of zebrafish length before and after treatment. Mean ± SD. n = 14–15. (E) mGFP and TagBFP expression in 4 dpf embryos treated with vehicle or 10 nM Alfa. Scale bar, 500 μm. (F) Quantified body length of two independent ubb:cyp24a1 lines and WT siblings at 4 dpf. Mean ± SD, Mann-Whitney test. ∗p < 0.05. n = 14–23. (G) cyp24a1mGFP expression in 1 μM Alfa-treated embryos. (H) Quantification of relative growth of 4 dpf embryos treated with vehicle or Alfa for 24 h. Mean ± SD, Student’s t test. n = 13. (I) Representative images and body length quantification of 6 mpf zebrafish. mpf, months post-fertilization. Mean ± SD, Student's t test. n = 7. Scale bar, 5 mm. (J) mGFP and TagBFP expression of 3 dpf embryos after a single heat-shock and 24-h drug treatment. Scale bar, 500 μm. (K) Quantified relative growth of 4 dpf embryos after a heat shock and 24-h drug treatment. Mean ± SD, Student’s t test. n = 10.
News
Upcoming Meetings
Zebrafish-Related Job Announcements
About ZFIN
The Zebrafish Information Network (ZFIN) is the database of genetic and genomic data for the zebrafish (Danio rerio) as a model organism. ZFIN provides a wide array of expertly curated, organized and cross-referenced zebrafish research data.
Learn MoreAdditional Resources
New Data in ZFIN
Fig. 6 of Savage et al., 2019
tmem33 knockdown reduces endothelial Notch and ERK signalling during angiogenesis. a–c Notch reporter expression is unaffected by injection of 0.4 ng tmem33 morpholinos at 26 hpf. Notch signalling activity in control embryos is present in neural tube (blue arrowhead) and DA (red arrowhead) (c, unpaired t-test; t = 0.5553; DF = 20; 2 repeats; n = 5 or 6 embryos per group). Scale bars 50 µm. d–f Injection of 0.4 ng tmem33 morpholinos reduces Notch reporter expression at 48 hpf. Notch expression in control Tg(csl:venus) embryos is present in the neural tube (blue arrowhead), DA (red arrowhead) and SeAs (white arrowheads) (f, unpaired t-test; p = 0.0451; t = 2.138; DF = 20; 2 repeats; n = 6 and 4 embryos per group). Scale bars 50 µm. g Expression of notch1b, dll4, hey2 and her12 are not significantly altered by tmem33 CRISPRi at 26 hpf (one-way ANOVA using post hoc Tukey’s comparison test. n = 3 repeats). h Expression of notch1b, dll4, hey2 and her12 are significantly reduced at 48 hpf by tmem33 CRISPRi (one-way ANOVA using post hoc Tukey’s comparison test. *p = < 0.05; **p = < 0.01. n = 3 repeats). i–p In comparison with control morphants (i–l), embryos injected with 0.4 ng tmem33 morpholino (m–p) display reduced expression of notch1b within the DA (i, m, red arrowheads) and SeAs (i, m, white arrowheads), dll4 within SeAs (j, n, white arrowheads), hey2 within the DA (k, o, red arrowheads) and her12 within the DA (l, p, red arrowheads) and SeAs (l, p, white arrowheads). Scale bars 100 µm. q–t tmem33 knockdown by CRISPRi reduces endothelial ERK phosphorylation (q, r, SeAs highlighted by yellow outline and white arrowheads). Intensity plot of ERK staining is shown (s, t, SeAs highlighted by yellow outline and white arrowheads). Scale bars 50 µm. u tmem33 crispants display significantly reduced levels of pERK phosphorylation. Pixel intensity normalised to neural tube ERK fluorescence (unpaired t-test, **p = 0.0097, t = 2.993 DF = 14. n = 2 repeats, 4 embryos per group). Source data are provided as a Source Data file
Fig. 4 of Sahu et al., 2019
Reduced tyrosine hydroxylase immunoreactivity in both the morphants and mutants at 5 dpf. (A) (a–d) TH1 immunohistochemistry revealed a loss of the neuronal population in the diencephalic cluster (5,6,11 cell group) in the Ntrk2b and Ntrk2a morphant. The neuronal cell group affected has been encircled. (A) (a′–d′): Higher magnification images of the affected TH cell group. (B) Total cell counts in the diencephalic region of the morphants. (C) The mutants have reduced TH positive cells in the same cell group and could be rescued by mRNA overexpression. (C) (a′–d′) Higher magnification images of the affected TH cell group. (D) TH cell counts from the mutants in the 5,6,11 cell group. (Bars represent Mean ± SEM, one-way ANOVA, Kruskal-Wallis test **p-value < 0.008, ****p-value < 0.0002, Scale bar = 100 um).
Fig. 7 of Villani et al., 2019
Gastrosomal Defects Affect Microglial Functionality (A) 4 dpf wild-type Tg(mpeg:GFP-caax) microglia stained with Nile Blue (cyan) in an embryo treated with Camptothecin to increase apoptosis. Scale bar, 5 μm. The white dotted line marks the gastrosome. (B) SPIM time-lapse of representative 4 dpf wild-type Tg(mpeg:GFP-caax) microglia stained with Nile Blue (cyan) in an embryo treated with Camptothecin to increase apoptosis. Scale bar, 10 μm. The white dotted line marks the shrinking gastrosome. See also Video S8. (C) Quantification of microglia responding to an injury in wild-type and blbNY007 microglia at different developmental stages; wt, 3.5 dpf, n = 20; blbNY007, 3.5 dpf, n = 20; wt, 4 dpf, n = 20; and blbNY007, 4 dpf, n = 16; whiskers: 5th/95th percentile, p value blb embryo). (D) Quantification of engulfment duration in wild-type (n = 20) and blbNY007 microglia (n = 11), whiskers: 5th/95th percentile, p value (E) RAW264.7 macrophages unfed (left column) or fed with HK H2B mCherry cells and fixed 24 h after apoptosis induction (right column). Slc37a2 antibody staining in untreated controls (upper panels) and in cells transfected with an siRNA targeting Slc37a2. (F) Quantification of the gastrosomal size (μm) in RAW macrophages fed with apoptotic HeLa cells in the absence or in the presence of Slc37a2 siRNA, p value < 0.0001. Representative images of this experiment in Figure S3A (yellow arrowheads).
Fig. 4 of Zhang et al., 2019
Defective tooth phenotypes in clcn7-deficient zebrafish. (A) Alcian blue and alizarin red staining results of 5thceratobranchial arch and teeth in control and clcn7 morphants at 5dpf. The malformed teeth were fewer with weak red staining clcn7 morphants. (B) Quantitative comparison of the extent of calcification among WT embryos, control and clcn7 morphants. (C) Comparison of embryonic tooth number. WT and control embryos had 3V1, 4V1 and 5V1 teeth, while clcn7 morphants showed 3V1, 4V1 and 5V1 fewer teeth. (D) Ultrastructure of tooth 4V1 in control and clcn7morphants. clcn7 morphants had malformed tooth and enameloid dysplasia. Red arrows point to the pits on the enameloid surface. For A, B, D: WT n=50, Control MO n=50, clcn7 MO n=50. The white square in the first image of figure A is the region for measuring calcified content in panel B. Error bar represents the SD. The experiment was repeated thrice with the same conditions. The data in image C was one of the representative experimental results. WT n=300, Control MO n=320, clcn7 MO n=300. ** p<0.01, *** p<0.001. Scale bars: 100 μm.
Fig. 4 of Kumar et al., 2019
WISH distribution analysis of zic3 in peli1bknockdown embryos at 14 hpf. Lateral view of zebrafishembryos (A–C). Anterior view (D–F). Posterior view (G–I). WT embryos (A, D, & G), 5′ mismatch controls (B, E, & H), and peli1b morphants injected with 10 ng morpholino at the 1-cell stage (C, F, & I). Red arrowheads show zic3expression and intensity in WT, 5′ mismatch, and peli1bmorphants. (n = 3). Abbreviations: pd- posterior diencephalon, dsc- dorsal spinal cord, dnp- dorsal neural plate, hb- hindbrain, mb- midbrain, dpnp-dorsal posterior neural plate, sp-segmental plate. Scale bar- 50 μm. (For interpretation of the references to color in this figure legend, the reader is referred to the web version of this article.)
Fig. 3 of Zhang et al., 2019
Craniofacial bone and cartilage abnormalities in clcn7 morphants. (A) Craniofacial phenotype comparison between control and clcn7 morphants. Cranial cartilages (blue) and mineralized bones (red) were stained with alcian blue and alizarin red in control and clcn7 morphants at 5 dpf, respectively. (A-C) Compared to WT and Control embryos, clcn7 morphants showed more malformed craniofacial skeletons, and clcn7 mRNA rescued the abnormalities in craniofacial region. (D, E) Abnormal ceratohyal (Ch) angle and altered location of otolith in clcn7 morphants. (F)Quantitative analysis of a series of changes of phenotypic indexes. clcn7 morphants showed obvious changes in the pattern of craniofacial structure. (G) WISH analysis showed the abolished expression of sp7 and col10a1 in cranial skeleton, most notably in the parasphenoid (Ps) and opercle (Op) bones in clcn7 morphants at 3 dpf. (H) Q-PCR analysis confirmed the reduced level of sp7 and col10a1. For A-E, WT n=300, Control MO n=320, clcn7 MO n=300, clcn7 MO + mRNA n=182. For H: Control MO n=50, clcn7 MO n=50. The red arrow indicates abnormal Ch angle, and the white arrow points to abnormal otolith. Ch: ceratohyal. M: Meckel's. Op: opercle. Pq: palatoquadrate. Ps: parasphenoid. WT: wide type. Error bar represents the SD. The experiment was repeated at least thrice with the same conditions. * p<0.05, ** p<0.01, *** p<0.001. Scale bars: 100 μm.
Fig. 3 of Villani et al., 2019
Cloning and Characterization of Slc37a2, the Gene Underlying the blb Phenotype (A) Schematic of the slc37a2 locus. Sequences of the NY007/t30301 allele (C/T mutation) and NA150/t30913 allele (T/A mutation). (B) Dorsal view of a 4 dpf Slc37a2 knockout generated with CRISPR-Cas9 as shown in (A). Scale bar, 30 μm. (C) Dorsal view of a representative immunostaining of a 4 dpf embryo where microglia are in green Tg(mpeg:GFP-caax) and Slc37a2 in red. Scale bar, 30 μm. (D) Magnification of (C). Scale bar, 15 μm. The yellow arrow points to a phagosome positive for Slc37a2. (E) Western blot analysis of Slc37a2 (55 kDa) and Tubulin (48 kDa) in wild-type, blbNY007, and blbNI150. (F) Immunostainings of Slc37a2 (cyan) and Lamp1 (red) in RAW264.7. Scale bar, 5 μm. (G and H) Mass-spectrometry data showing normalized intensities of glucose 6-phosphate (G) not significant, and D-gluconate-6-phosphate (H) significant, p value < 0.0001, in blbNY007 and wild-type.
Fig. 5 of Cal et al., 2019
Detailed visualization of ventral pigment cells in WT and asip1 mutants. (A) Ventral view of 210 dpf WT belly. (B) Belly of 210 dpf WT fish carrying Tg(Kita:GalTA4;UAS:mCherry) (labels melanophores) transgene shows no melanophores in ventral skin. (C) Ventral view of 210 dpf asip1K.O. belly. (D) Belly of 210 dpf asip1K.O. fish carrying Tg(Kita:GalTA4;UAS:mCherry) transgene shows high number of melanophores in ventral skin. (E) Internal view of 210 dpf WT abdominal wall shows a white sheet of iridophores with few internal melanophores (black arrow). (F) Abdominal wall of 210 dpf WT fish carrying Tg(TDL358:GFP) (labels iridophores and glia) transgene displays a uniform and continuous sheet of iridophores. (G) Internal view of 210 dpf asip1K.O. abdominal wall shows a disrupted and discontinuous sheet of iridophores with high number of melanophores (black arrow) and some xanthophores (orange arrow). (H) Abdominal wall of 210 dpf asip1K.O. fish carrying Tg(TDL358:GFP)transgene exhibits a broken sheet of iridophores. Scale bars: 100 μm.
Fig. 6 of Huo et al., 2019
Expression of cancer angiogenesis genes in TANs and effects of neutrophil depletion on liver tumorigenesis and angiogenesis. (A) Heatmap representation of expression of cancer angiogenesis genes extracted from DEGs of TANs. The color codes represent fold changes of expression of each gene in each sample relative to the mean expression of all samples. The list of cancer angiogenesis genes was obtained based on IPA knowledge datbase. (B) Representative confocal images of 6-dpf lyz+ larvae injected with different morpholinos: MO_SC (left, n = 18) or MO_gcsfr (right, n = 20). (C) Numbers of neutrophils in the middle body after injection of morpholinos. Neutrophils were counted in the the middle body surrounding the liver region (from the posterior edge of eye to posterior edge of swimbladder). (D) Representative 3D confocal images of 6-dpf kras−/fli+ and kras+/fli+ larvae injected with MO_SC or MO_gcsfr. For fli+ larvae, both Tg(fli1a::GFP) (left) and Tg(fli1a::RFP) (middle and right) were used. Kras- larvae were LiPan strain (left) with DsRed expression in the liver. (C and D) Quantification of blood vessel density in the liver area (E) and liver size (F) after morpholino injection. N >20 in each group. Statistical significance: *p < 0.05.
Fig. 2 of Han et al., 2019
Vitamin D Signaling Enhances Organismal Size (A) MIP images and quantification of H3P staining of 3 dpf embryos. hpt, hours post-treatment; H3P, phospho-Histone H3. Mean ± SD, Mann-Whitney test and Student's t test. ∗∗∗∗p < 0.0001. n = 11–13. Scale bar, 500 μm. (B) Example and quantification of 4 dpf zebrafish growth. Mean ± SD, Mann-Whitney test and Student’s t test. ∗∗p < 0.01; ∗∗∗p < 0.001. n = 12-14. Scale bar, 500 μm. (C) Growth and rescue of 2 mpf juvenile wild-type (WT) and ubb:cyp24a1 zebrafish. Scale bar, 4 mm. (D) Quantification of zebrafish length before and after treatment. Mean ± SD. n = 14–15. (E) mGFP and TagBFP expression in 4 dpf embryos treated with vehicle or 10 nM Alfa. Scale bar, 500 μm. (F) Quantified body length of two independent ubb:cyp24a1 lines and WT siblings at 4 dpf. Mean ± SD, Mann-Whitney test. ∗p < 0.05. n = 14–23. (G) cyp24a1mGFP expression in 1 μM Alfa-treated embryos. (H) Quantification of relative growth of 4 dpf embryos treated with vehicle or Alfa for 24 h. Mean ± SD, Student’s t test. n = 13. (I) Representative images and body length quantification of 6 mpf zebrafish. mpf, months post-fertilization. Mean ± SD, Student's t test. n = 7. Scale bar, 5 mm. (J) mGFP and TagBFP expression of 3 dpf embryos after a single heat-shock and 24-h drug treatment. Scale bar, 500 μm. (K) Quantified relative growth of 4 dpf embryos after a heat shock and 24-h drug treatment. Mean ± SD, Student’s t test. n = 10.