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 More
Additional Resources
Data Mining
Browse Genome
Order cDNAs and ESTs
New Data in ZFIN
Fig. 1 of Wong et al., 2021
Aberrant mvda function causes developmental defects in zebrafish. A Quantitative real-time PCR (qRT-PCR) for twelve embryo development stages (0.2 hpf, 1 hpf, 2 hpf, 3.7 hpf, 6 hpf, 24 hpf, 30 hpf, 48 hpf, 72 hpf, 96 hpf, 120 hpf, and 144 hpf) demonstrates different expression patterns of mvda during embryonic development. B Effectiveness of mvda knockdown was confirmed by RT-PCR and sanger sequencing. The zebrafish mvda gene was targeted by specific morpholino antisense to prevent the proper splicing of exon 3 (E3I3-MO). Primers spanning mvda exon 1 (forward) and exon 4 (reverse) interrogate the presence of wild type (non-mutant) transcripts or those in which intron 3 has been inserted. RT-PCR of mvda transcript from control-MO and E3I3-MO injected embryos at 2-dpf, demonstrating insertion of intron 3. Sanger sequencing of both the wild-type band and the intron 3-inserted band validating the wild-type sequence and the intron 3-inserted sequence. C–J Gross morphology at 2-dpf and 4-dpf. Compared with the control group, knockdown of mvda presented hydrocephaly (E, blue arrowhead), eye defects (E, I, blue arrow), pericardial oedema (E, I, red arrow), blood accumulation in the caudal vein (E, F, red circled area), and skin defects (J, black arrows). Heartbeat and circulation in the caudal vein were visible in the control fish but were abnormal in mvda morphants (Additional file 2: Video S1, Additional file 3: Video S2). hpf, hours post fertilization; dpf, days post fertilization. Scale bars = 100 µm
FIGURE 1 of Wiweger et al., 2021
Zebrafish npc2 mutant. (A) Multiple species alignments demonstrated high conservation of the NPC2 protein among vertebrates. Arrows indicate positions of the mutation. (B) Expression levels of the npc2 gene in different tissues in adult fish. Expression was normalized to tissue with the lowest expression (brain). (C) Chromatograms confirmed a small deletion in the npc2 mutant. (D) Graphical representation of melt profiles in wildtypes (black), heterozygous mutants (blue), and homozygous mutants (gray) that originated from fish after incrossing npc2±. (E) mRNA levels of the npc2 gene in various organs in npc2–/– zebrafish relative to wildtype controls. The data are expressed as the mean ± SEM of three 9-month-old fish per group. Error bars represent the SEM. ***p < 0.001 and **p < 0.01. (F) Wildtype, heterozygous, and homozygous npc2 mutants had indistinguishable phenotypes at 5 dpf. Scale = 1 mm. (G) Morphology of adult fish. Smaller body size and weight in 8-month-old npc2–/– fish and indistinguishable phenotype of npc2±. Error bars represent the SD.
Figure 2 of Ghilardi et al., 2021
smpx knockdown disturbs the proper fiber arrangement during development. (A–D) side views, anterior left, dorsal top. Paraffin sections of Control-MO (A,C) and smpx-MO (B,D) injected embryos at 48 hpf (A,B) and 4 dpf (C,D). The red asterisks indicate alterations in the muscle array. (E–H) side views, anterior left, dorsal top. Confocal Z-stacks taken from whole-mount embryos (48 hpf) and larvae (72 hpf) labelled with (E,F) myosin heavy chain (MHC) antibody for slow fibers and (G,H) phalloidin (act) for actin filaments of the fast fibers. The red (F) and white (H) asterisks indicate alterations in the normal muscle array (controls in (E,G), respectively). (I,J) representative lateral view of an embryo injected with the construct encoding the Smpx:GFP chimera (see Figure S1A for construct details); muscle fibers (arrowhead) and epithelial cells (arrow) are both uniformly painted with no accumulation of Smpx:GFP in the nuclei. Inset: magnification of a slow fiber with the nucleus (asterisk) labelled with DAPI (blue). Anterior left, dorsal top. Scale bars = 25 μm in (A–D); 20 μm in (E,F); 20 μm in (G,H); 100 μm in (I,J).
FIGURE 9 of Wiweger et al., 2021
Signs of inflammation and alterations of Ca2+ homeostasis in npc2–/– zebrafish. Scatterplots show the normalized expression of selected genes in brain and liver tissue from 9-month-old npc2–/– homozygotes and wildtype zebrafish. Each circle corresponds to one zebrafish. The 18S ribosomal gene was used as a reference. Samples from at least three fish were analyzed. ***p < 0.001, **p < 0.01, and *p < 0.05.
Figure 1 of Ghilardi et al., 2021
Phenotypical and ear defects in smpx zebrafish morphants (MO). (A,B) representative phenotype caused by the lack of Smpx. Control-MO (A) and smpx-MO (B) injected embryos. The red arrow points to the downward trunk/tail curvature indicative of cilia disfunction. (C–F) kinocilia of the anterior (ac), lateral (lc) and posterior (pc) cristae of the inner ear of 72 hpf (C,D) and 5 dpf (E,F) larvae injected with ctrl- (C,E) and smpx-MO (D,F). Cristae kinocilia are stained with the antibody against acetylated tubulin (ac tub); phalloidin is used to label the actin (act) of the stereocilia. White arrowheads indicate the different ‘posture’ of the lateral crista kinocilia. (G,H) SEM images of the ciliary bundle in the control larvae (G) and smpx morphants (H). The arrowhead indicates the kinocilium, with the arrow the stereocilia. (I,J) representative confocal images of the otic cavity injected with FM4-64, labeling the inner ear hair cells in the control larvae ((I), n = 4) and smpx morphants ((J), n = 7). The asterisks indicate the lack of signal in the ac, lc and pc of the Smpx-deficient larvae, suggestive of an impaired mechanotransduction. (I’) magnified view of the anterior crista in (I) (white rectangle). Scale bars = 50 μm in (C–F); 25 μm in (I,J); 1 μm in (G,H).
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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 More
Additional Resources
Data Mining
Browse Genome
Order cDNAs and ESTs
New Data in ZFIN
Fig. 1 of Wong et al., 2021
Aberrant mvda function causes developmental defects in zebrafish. A Quantitative real-time PCR (qRT-PCR) for twelve embryo development stages (0.2 hpf, 1 hpf, 2 hpf, 3.7 hpf, 6 hpf, 24 hpf, 30 hpf, 48 hpf, 72 hpf, 96 hpf, 120 hpf, and 144 hpf) demonstrates different expression patterns of mvda during embryonic development. B Effectiveness of mvda knockdown was confirmed by RT-PCR and sanger sequencing. The zebrafish mvda gene was targeted by specific morpholino antisense to prevent the proper splicing of exon 3 (E3I3-MO). Primers spanning mvda exon 1 (forward) and exon 4 (reverse) interrogate the presence of wild type (non-mutant) transcripts or those in which intron 3 has been inserted. RT-PCR of mvda transcript from control-MO and E3I3-MO injected embryos at 2-dpf, demonstrating insertion of intron 3. Sanger sequencing of both the wild-type band and the intron 3-inserted band validating the wild-type sequence and the intron 3-inserted sequence. C–J Gross morphology at 2-dpf and 4-dpf. Compared with the control group, knockdown of mvda presented hydrocephaly (E, blue arrowhead), eye defects (E, I, blue arrow), pericardial oedema (E, I, red arrow), blood accumulation in the caudal vein (E, F, red circled area), and skin defects (J, black arrows). Heartbeat and circulation in the caudal vein were visible in the control fish but were abnormal in mvda morphants (Additional file 2: Video S1, Additional file 3: Video S2). hpf, hours post fertilization; dpf, days post fertilization. Scale bars = 100 µm
FIGURE 1 of Wiweger et al., 2021
Zebrafish npc2 mutant. (A) Multiple species alignments demonstrated high conservation of the NPC2 protein among vertebrates. Arrows indicate positions of the mutation. (B) Expression levels of the npc2 gene in different tissues in adult fish. Expression was normalized to tissue with the lowest expression (brain). (C) Chromatograms confirmed a small deletion in the npc2 mutant. (D) Graphical representation of melt profiles in wildtypes (black), heterozygous mutants (blue), and homozygous mutants (gray) that originated from fish after incrossing npc2±. (E) mRNA levels of the npc2 gene in various organs in npc2–/– zebrafish relative to wildtype controls. The data are expressed as the mean ± SEM of three 9-month-old fish per group. Error bars represent the SEM. ***p < 0.001 and **p < 0.01. (F) Wildtype, heterozygous, and homozygous npc2 mutants had indistinguishable phenotypes at 5 dpf. Scale = 1 mm. (G) Morphology of adult fish. Smaller body size and weight in 8-month-old npc2–/– fish and indistinguishable phenotype of npc2±. Error bars represent the SD.
Figure 2 of Ghilardi et al., 2021
smpx knockdown disturbs the proper fiber arrangement during development. (A–D) side views, anterior left, dorsal top. Paraffin sections of Control-MO (A,C) and smpx-MO (B,D) injected embryos at 48 hpf (A,B) and 4 dpf (C,D). The red asterisks indicate alterations in the muscle array. (E–H) side views, anterior left, dorsal top. Confocal Z-stacks taken from whole-mount embryos (48 hpf) and larvae (72 hpf) labelled with (E,F) myosin heavy chain (MHC) antibody for slow fibers and (G,H) phalloidin (act) for actin filaments of the fast fibers. The red (F) and white (H) asterisks indicate alterations in the normal muscle array (controls in (E,G), respectively). (I,J) representative lateral view of an embryo injected with the construct encoding the Smpx:GFP chimera (see Figure S1A for construct details); muscle fibers (arrowhead) and epithelial cells (arrow) are both uniformly painted with no accumulation of Smpx:GFP in the nuclei. Inset: magnification of a slow fiber with the nucleus (asterisk) labelled with DAPI (blue). Anterior left, dorsal top. Scale bars = 25 μm in (A–D); 20 μm in (E,F); 20 μm in (G,H); 100 μm in (I,J).
FIGURE 9 of Wiweger et al., 2021
Signs of inflammation and alterations of Ca2+ homeostasis in npc2–/– zebrafish. Scatterplots show the normalized expression of selected genes in brain and liver tissue from 9-month-old npc2–/– homozygotes and wildtype zebrafish. Each circle corresponds to one zebrafish. The 18S ribosomal gene was used as a reference. Samples from at least three fish were analyzed. ***p < 0.001, **p < 0.01, and *p < 0.05.
Figure 1 of Ghilardi et al., 2021
Phenotypical and ear defects in smpx zebrafish morphants (MO). (A,B) representative phenotype caused by the lack of Smpx. Control-MO (A) and smpx-MO (B) injected embryos. The red arrow points to the downward trunk/tail curvature indicative of cilia disfunction. (C–F) kinocilia of the anterior (ac), lateral (lc) and posterior (pc) cristae of the inner ear of 72 hpf (C,D) and 5 dpf (E,F) larvae injected with ctrl- (C,E) and smpx-MO (D,F). Cristae kinocilia are stained with the antibody against acetylated tubulin (ac tub); phalloidin is used to label the actin (act) of the stereocilia. White arrowheads indicate the different ‘posture’ of the lateral crista kinocilia. (G,H) SEM images of the ciliary bundle in the control larvae (G) and smpx morphants (H). The arrowhead indicates the kinocilium, with the arrow the stereocilia. (I,J) representative confocal images of the otic cavity injected with FM4-64, labeling the inner ear hair cells in the control larvae ((I), n = 4) and smpx morphants ((J), n = 7). The asterisks indicate the lack of signal in the ac, lc and pc of the Smpx-deficient larvae, suggestive of an impaired mechanotransduction. (I’) magnified view of the anterior crista in (I) (white rectangle). Scale bars = 50 μm in (C–F); 25 μm in (I,J); 1 μm in (G,H).