Embryonic Senescence and Laminopathies in a Progeroid Zebrafish Model
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{"title"=>"Embryonic senescence and laminopathies in a progeroid zebrafish model", "type"=>"journal", "authors"=>[{"first_name"=>"Eriko", "last_name"=>"Koshimizu", "scopus_author_id"=>"24833144800"}, {"first_name"=>"Shintaro", "last_name"=>"Imamura", "scopus_author_id"=>"8616936900"}, {"first_name"=>"Jie", "last_name"=>"Qi", "scopus_author_id"=>"57198485704"}, {"first_name"=>"Jamal", "last_name"=>"Toure", "scopus_author_id"=>"35084393000"}, {"first_name"=>"Delgado M.", "last_name"=>"Valdez", "scopus_author_id"=>"8878803000"}, {"first_name"=>"Christopher E.", "last_name"=>"Carr", "scopus_author_id"=>"7202450021"}, {"first_name"=>"Jun ichi", "last_name"=>"Hanai", "scopus_author_id"=>"13310370700"}, {"first_name"=>"Shuji", "last_name"=>"Kishi", "scopus_author_id"=>"7102539885"}], "year"=>2011, "source"=>"PLoS ONE", "identifiers"=>{"sgr"=>"79953303050", "doi"=>"10.1371/journal.pone.0017688", "pui"=>"361543627", "pmid"=>"21479207", "scopus"=>"2-s2.0-79953303050", "issn"=>"19326203", "isbn"=>"1932-6203 (Electronic)\r1932-6203 (Linking)"}, "id"=>"fef4c2eb-0f22-38c6-9e3b-94039d02e4ce", "abstract"=>"Mutations that disrupt the conversion of prelamin A to mature lamin A cause the rare genetic disorder Hutchinson-Gilford progeria syndrome and a group of laminopathies. Our understanding of how A-type lamins function in vivo during early vertebrate development through aging remains limited, and would benefit from a suitable experimental model. The zebrafish has proven to be a tractable model organism for studying both development and aging at the molecular genetic level. Zebrafish show an array of senescence symptoms resembling those in humans, which can be targeted to specific aging pathways conserved in vertebrates. However, no zebrafish models bearing human premature senescence currently exist.", "link"=>"http://www.mendeley.com/research/embryonic-senescence-laminopathies-progeroid-zebrafish-model", "reader_count"=>74, "reader_count_by_academic_status"=>{"Professor > Associate Professor"=>5, "Researcher"=>27, "Student > Doctoral Student"=>3, "Student > Ph. D. Student"=>16, "Student > Postgraduate"=>2, "Student > Master"=>6, "Other"=>3, "Student > Bachelor"=>8, "Professor"=>4}, "reader_count_by_user_role"=>{"Professor > Associate Professor"=>5, "Researcher"=>27, "Student > Doctoral Student"=>3, "Student > Ph. D. Student"=>16, "Student > Postgraduate"=>2, "Student > Master"=>6, "Other"=>3, "Student > Bachelor"=>8, "Professor"=>4}, "reader_count_by_subject_area"=>{"Engineering"=>1, "Unspecified"=>1, "Biochemistry, Genetics and Molecular Biology"=>17, "Agricultural and Biological Sciences"=>42, "Medicine and Dentistry"=>5, "Neuroscience"=>3, "Veterinary Science and Veterinary Medicine"=>1, "Physics and Astronomy"=>1, "Social Sciences"=>2, "Immunology and Microbiology"=>1}, "reader_count_by_subdiscipline"=>{"Engineering"=>{"Engineering"=>1}, "Medicine and Dentistry"=>{"Medicine and Dentistry"=>5}, "Neuroscience"=>{"Neuroscience"=>3}, "Social Sciences"=>{"Social Sciences"=>2}, "Physics and Astronomy"=>{"Physics and Astronomy"=>1}, "Immunology and Microbiology"=>{"Immunology and Microbiology"=>1}, "Agricultural and Biological Sciences"=>{"Agricultural and Biological Sciences"=>42}, "Biochemistry, Genetics and Molecular Biology"=>{"Biochemistry, Genetics and Molecular Biology"=>17}, "Unspecified"=>{"Unspecified"=>1}, "Veterinary Science and Veterinary Medicine"=>{"Veterinary Science and Veterinary Medicine"=>1}}, "reader_count_by_country"=>{"United States"=>2, "Japan"=>2, "Finland"=>1, "Poland"=>1, "United Kingdom"=>1, "France"=>1, "Portugal"=>1}, "group_count"=>2}

Scopus | Further Information

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Figshare

  • {"files"=>["https://ndownloader.figshare.com/files/787474"], "description"=>"<p>N.A.: not applied or analyzed in this study.</p><p>*Antibody-mediated detection.</p><p>**Dye-mediated detection.</p><p>***Phenotype-specific assay.</p>", "links"=>[], "tags"=>["zebrafish", "models", "laminopathy"], "article_id"=>457837, "categories"=>["Chemistry"], "users"=>["Eriko Koshimizu", "Shintaro Imamura", "Jie Qi", "Jamal Toure", "Delgado M. Valdez Jr", "Christopher E. Carr", "Jun-ichi Hanai", "Shuji Kishi"], "doi"=>"https://dx.doi.org/10.1371/journal.pone.0017688.t002", "stats"=>{"downloads"=>3, "page_views"=>9, "likes"=>0}, "figshare_url"=>"https://figshare.com/articles/_Summary_of_distinct_zebrafish_models_for_laminopathy_in_this_study_/457837", "title"=>"Summary of distinct zebrafish models for laminopathy in this study.", "pos_in_sequence"=>0, "defined_type"=>3, "published_date"=>"2011-03-30 02:10:37"}
  • {"files"=>["https://ndownloader.figshare.com/files/787404"], "description"=>"<p>A shorter lifespan in z<i>progerin</i> and z<i>prelamin A</i> transgenic zebrafish is demonstrated by Kaplan-Meier survival analysis. In z<i>progerin</i> transgenic zebrafish (Progerin Tg), two independent cohorts (Cohort 1 and 2) were analyzed and the survival curves show significant decreases in lifespan compared with the corresponding wild-type siblings (Non-Tg siblings). z<i>Prelamin A</i> transgenic zebrafish (Prelamin Tg) also showed a relatively shorter lifespan than their siblings (Non-Tg siblings).</p>", "links"=>[], "tags"=>["lifespan", "transgenic"], "article_id"=>457773, "categories"=>["Chemistry"], "users"=>["Eriko Koshimizu", "Shintaro Imamura", "Jie Qi", "Jamal Toure", "Delgado M. Valdez Jr", "Christopher E. Carr", "Jun-ichi Hanai", "Shuji Kishi"], "doi"=>"https://dx.doi.org/10.1371/journal.pone.0017688.g008", "stats"=>{"downloads"=>1, "page_views"=>4, "likes"=>0}, "figshare_url"=>"https://figshare.com/articles/_Demographic_analysis_of_the_lifespan_in_zprogerin_and_zprelamin_A_transgenic_zebrafish_/457773", "title"=>"Demographic analysis of the lifespan in <i>zprogerin</i> and <i>zprelamin A</i> transgenic zebrafish.", "pos_in_sequence"=>0, "defined_type"=>1, "published_date"=>"2011-03-30 02:09:33"}
  • {"files"=>["https://ndownloader.figshare.com/files/787272"], "description"=>"<p>(<b>A</b>) External features of z<i>progerin</i> transgenic zebrafish (30 hpf) without (Control, -FTI) or with FTI treatment (100 µM, +FTI). (<b>B</b>) Amelioration of nuclear morphology by FTI treatment (100 µM, +FTI) in comparison with untreated (-FTI) z<i>progerin</i> fish. Analysis of the misshapen nuclear morphology was also performed by using different concentrations of FTI in z<i>progerin</i> transgenic embryos at 30 hpf as shown in right graph. The number of cells with abnormally shaped nuclei were determined by fluorescence microscopy (*<i>P</i><0.05). (<b>C</b>) Amelioration of muscle phenotype (stained with the F59 antibody) at 24 hpf and reduction of SA-β-gal activity at 3.5 dpf in z<i>progerin</i> fish embryos by FTI treatment (100 µM, +FTI) in comparison with the untreated condition (-FTI). (<b>D</b>) Western blot analysis of prelamin A accumulations in AB9 zebrafish fibroblasts following FTI treatment, and the quantitation of prelamin A amounts in right graph. The quantifications of intrinsic prelamin A accumulations were shown are the averages from two-independent experiments.</p>", "links"=>[], "tags"=>["transgenic"], "article_id"=>457640, "categories"=>["Chemistry"], "users"=>["Eriko Koshimizu", "Shintaro Imamura", "Jie Qi", "Jamal Toure", "Delgado M. Valdez Jr", "Christopher E. Carr", "Jun-ichi Hanai", "Shuji Kishi"], "doi"=>"https://dx.doi.org/10.1371/journal.pone.0017688.g007", "stats"=>{"downloads"=>1, "page_views"=>12, "likes"=>0}, "figshare_url"=>"https://figshare.com/articles/_FTI_treatment_of_z_progerin_zlamin_A_916_37_transgenic_zebrafish_/457640", "title"=>"FTI treatment of z<i>progerin/zlamin A-Δ37</i> transgenic zebrafish.", "pos_in_sequence"=>0, "defined_type"=>1, "published_date"=>"2011-03-30 02:07:20"}
  • {"files"=>["https://ndownloader.figshare.com/files/786914"], "description"=>"<p>(<b>A</b>) Muscle fiber visualization in zlamin A/C-knockdown embryos. (a–d) The left panels show a lateral view of the entire embryo bodies and a magnified bright field view of the somites. (e–h) Lateral views of MO-injected embryos at 24 hpf stained with the F59 antibody (adaxial cells/slow muscle fibers). In panel (f), white arrowheads indicate broken or missing muscle fibers. In panel (h), white arrowheads indicate the wavy muscle fibers in compared with control embryos. (i–l) The right panels show cryostat sections of 48 hpf <i>LMNA</i>-MO injected embryos stained for fast muscle fibers (F310). (<b>B</b>) Percentage of muscle phenotypes scored for MO-injected embryos at 24 hpf. The graph shows the distribution of phenotypes observed following injections with 4 ng of MOs. Migration failure in embryos is represented in gray and wavy muscle fibers in black. The percentage of each muscle phenotypes ‘waving’, ‘migration failure’, ‘normal’ were, respectively, MO1-5mis; 7.5%, 5.0%, 87.5%; MO1-MO; 3.8%, 46.2%, 50.0%; MO2-5mis; 6.1%, 6.1%, 87.8%; MO2-MO; 29.4%, 25.5%, 45.1%. (<b>C</b>) Cartilage in 6 dpf larvae were stained with Alcian blue and then whole-mounted. (a–d) Lateral views of the head portions of living larvae are shown in the top panels. (e–h) Lateral view of Alcian blue stained larvae. (i–l) Ventral views of Alcian blue stained larvae. The red lines indicate the ceratohyal articulates (ch), and the red arrow indicates the Meckel's (m) to palatoquadrate (pq).</p>", "links"=>[], "tags"=>["knockdown", "zebrafish", "lamin", "induces", "laminopathies", "muscular", "dystrophy", "craniofacial"], "article_id"=>457269, "categories"=>["Chemistry"], "users"=>["Eriko Koshimizu", "Shintaro Imamura", "Jie Qi", "Jamal Toure", "Delgado M. Valdez Jr", "Christopher E. Carr", "Jun-ichi Hanai", "Shuji Kishi"], "doi"=>"https://dx.doi.org/10.1371/journal.pone.0017688.g004", "stats"=>{"downloads"=>1, "page_views"=>62, "likes"=>0}, "figshare_url"=>"https://figshare.com/articles/_The_knockdown_of_zebrafish_lamin_A_C_induces_laminopathies_associated_with_muscular_dystrophy_and_craniofacial_abnormalities_/457269", "title"=>"The knockdown of zebrafish lamin A/C induces laminopathies associated with muscular dystrophy and craniofacial abnormalities.", "pos_in_sequence"=>0, "defined_type"=>1, "published_date"=>"2011-03-30 02:01:09"}
  • {"files"=>["https://ndownloader.figshare.com/files/394258", "https://ndownloader.figshare.com/files/394282", "https://ndownloader.figshare.com/files/394306", "https://ndownloader.figshare.com/files/394333", "https://ndownloader.figshare.com/files/394355", "https://ndownloader.figshare.com/files/394370", "https://ndownloader.figshare.com/files/394389"], "description"=>"<div><h3>Background</h3><p>Mutations that disrupt the conversion of prelamin A to mature lamin A cause the rare genetic disorder Hutchinson-Gilford progeria syndrome and a group of laminopathies. Our understanding of how A-type lamins function <em>in vivo</em> during early vertebrate development through aging remains limited, and would benefit from a suitable experimental model. The zebrafish has proven to be a tractable model organism for studying both development and aging at the molecular genetic level. Zebrafish show an array of senescence symptoms resembling those in humans, which can be targeted to specific aging pathways conserved in vertebrates. However, no zebrafish models bearing human premature senescence currently exist.</p> <h3>Principal Findings</h3><p>We describe the induction of embryonic senescence and laminopathies in zebrafish harboring disturbed expressions of the lamin A gene (<em>LMNA</em>). Impairments in these fish arise in the skin, muscle and adipose tissue, and sometimes in the cartilage. Reduced function of lamin A/C by translational blocking of the <em>LMNA</em> gene induced apoptosis, cell-cycle arrest, and craniofacial abnormalities/cartilage defects. By contrast, induced cryptic splicing of <em>LMNA</em>, which generates the deletion of 8 amino acid residues lamin A (zlamin A-Δ8), showed embryonic senescence and S-phase accumulation/arrest. Interestingly, the abnormal muscle and lipodystrophic phenotypes were common in both cases. Hence, both decrease-of-function of lamin A/C and gain-of-function of aberrant lamin A protein induced laminopathies that are associated with mesenchymal cell lineages during zebrafish early development. Visualization of individual cells expressing zebrafish progerin (zProgerin/zlamin A-Δ37) fused to green fluorescent protein further revealed misshapen nuclear membrane. A farnesyltransferase inhibitor reduced these nuclear abnormalities and significantly prevented embryonic senescence and muscle fiber damage induced by zProgerin. Importantly, the adult Progerin fish survived and remained fertile with relatively mild phenotypes only, but had shortened lifespan with obvious distortion of body shape.</p> <h3>Conclusion</h3><p>We generated new zebrafish models for a human premature aging disorder, and further demonstrated the utility for studying laminopathies. Premature aging could also be modeled in zebrafish embryos. This genetic model may thus provide a new platform for future drug screening as well as genetic analyses aimed at identifying modifier genes that influence not only progeria and laminopathies but also other age-associated human diseases common in vertebrates.</p> </div>", "links"=>[], "tags"=>["embryonic", "senescence", "laminopathies", "progeroid", "zebrafish"], "article_id"=>137871, "categories"=>["Chemistry"], "users"=>["Eriko Koshimizu", "Shintaro Imamura", "Jie Qi", "Jamal Toure", "Delgado M. Valdez Jr", "Christopher E. Carr", "Jun-ichi Hanai", "Shuji Kishi"], "doi"=>["https://dx.doi.org/10.1371/journal.pone.0017688.s001", "https://dx.doi.org/10.1371/journal.pone.0017688.s002", "https://dx.doi.org/10.1371/journal.pone.0017688.s003", "https://dx.doi.org/10.1371/journal.pone.0017688.s004", "https://dx.doi.org/10.1371/journal.pone.0017688.s005", "https://dx.doi.org/10.1371/journal.pone.0017688.s006", "https://dx.doi.org/10.1371/journal.pone.0017688.s007"], "stats"=>{"downloads"=>7, "page_views"=>10, "likes"=>0}, "figshare_url"=>"https://figshare.com/articles/Embryonic_Senescence_and_Laminopathies_in_a_Progeroid_Zebrafish_Model/137871", "title"=>"Embryonic Senescence and Laminopathies in a Progeroid Zebrafish Model", "pos_in_sequence"=>0, "defined_type"=>4, "published_date"=>"2011-03-30 02:11:11"}
  • {"files"=>["https://ndownloader.figshare.com/files/787510"], "description"=>"<p>Cartilage defects in LMNA-MO-injected embryos.</p>", "links"=>[], "tags"=>["defects", "lmna-mo-injected"], "article_id"=>457878, "categories"=>["Chemistry"], "users"=>["Eriko Koshimizu", "Shintaro Imamura", "Jie Qi", "Jamal Toure", "Delgado M. Valdez Jr", "Christopher E. Carr", "Jun-ichi Hanai", "Shuji Kishi"], "doi"=>"https://dx.doi.org/10.1371/journal.pone.0017688.t001", "stats"=>{"downloads"=>2, "page_views"=>5, "likes"=>0}, "figshare_url"=>"https://figshare.com/articles/_Cartilage_defects_in_LMNA_MO_injected_embryos_/457878", "title"=>"Cartilage defects in LMNA-MO-injected embryos.", "pos_in_sequence"=>0, "defined_type"=>3, "published_date"=>"2011-03-30 02:11:18"}
  • {"files"=>["https://ndownloader.figshare.com/files/786784"], "description"=>"<p>(<b>A</b>) EGFP-zPrelamin A expression in zebrafish embryos. (<b>B</b>) EGFP-zlamin A-Δ8 expression in zebrafish embryos. (<b>C</b>) EGFP-zlamin A-Δ37/zProgerin expression in embryos. (<b>D</b>) The nuclear localization of EGFP-zPrelamin A and the nuclear morphology in the expressing cells within the embryo. (<b>E</b>) The nuclear localization of EGFP-zlamin A-Δ8 and the nuclear morphology in the expressing cells within the embryo. (<b>F</b>) The nuclear localization of EGFP-zlamin A-Δ37/zProgerin and nuclear morphology in the expressing cells within the embryo.</p>", "links"=>[], "tags"=>["egfp-tagged", "zprelamin", "zlamin", "zebrafish", "embryos", "morphologies", "expressing"], "article_id"=>457143, "categories"=>["Chemistry"], "users"=>["Eriko Koshimizu", "Shintaro Imamura", "Jie Qi", "Jamal Toure", "Delgado M. Valdez Jr", "Christopher E. Carr", "Jun-ichi Hanai", "Shuji Kishi"], "doi"=>"https://dx.doi.org/10.1371/journal.pone.0017688.g003", "stats"=>{"downloads"=>1, "page_views"=>7, "likes"=>0}, "figshare_url"=>"https://figshare.com/articles/_Expression_of_EGFP_tagged_zprelamin_A_zlamin_A_916_8_and_zlamin_A_916_37_zProgerin_in_zebrafish_embryos_and_the_nuclear_morphologies_in_the_expressing_cells_/457143", "title"=>"Expression of EGFP-tagged zprelamin A, zlamin A-Δ8, and zlamin A-Δ37/zProgerin in zebrafish embryos and the nuclear morphologies in the expressing cells.", "pos_in_sequence"=>0, "defined_type"=>1, "published_date"=>"2011-03-30 01:59:03"}
  • {"files"=>["https://ndownloader.figshare.com/files/786520"], "description"=>"<p>(<b>A</b>) The zebrafish <i>LMNA</i> gene was assigned to Linkage Group 16 (LG16) and is syntenic with human chromosome 1q21-23. Left: six genes including <i>LMNA</i> are located within a 10 Mb genomic region on human chromosome 1. Right: six zebrafish homologs of these genes are listed according to the map positions on LG16. (<b>B</b>) RT-PCR analysis of adult zlamin A revealing strong expression in the brain, heart, liver and muscle (upper panels). Western analysis of 6 dpf embryo lysates and 1-year old adult tissues was preformed using an anti-chicken lamin A polyclonal antibody (ab14309), as well as an anti-mouse actin monoclonal antibody as a loading control (lower panels). (<b>C</b>) Amino acid sequence alignment of the C-terminal portions in human (<i>Homo sapiens</i>) lamin A (Hs. lamin A) and zebrafish (<i>Danio rerio</i>) lamin A (Dr. lamin A) and their deleted forms (Δ50 in human; Δ37 and Δ8 in zebrafish) induced by cryptic splicing events. (<b>D</b>) External features of a wild-type non-transgenic sibling fish (<i>wt</i>; 1.5-year old). Two representative <i>zprogerin</i> transgenic fish with curved trunks (<i>zlamin A-Δ37</i>; 1.5-year old) are shown. A z<i>prelamin A</i> transgenic fish with a wavy trunk (2.1-year old) is also shown. In these transgenic fish, spinal curvatures and disproportional body shapes are prominently observed. Scale bars, 1 cm. Qualifications of the abnormal body shapes are shown in the right graph (cohorts of 18 months of age). (<b>E</b>) SA-β-gal staining of wild-type sibling and transgenic fish (1.9-year old). Quantifications of the SA-β-gal intensities in the fish are shown in the right graph (cohorts of 18 months of age, *<i>P</i><0.01).</p>", "links"=>[], "tags"=>["zebrafish", "prelamin"], "article_id"=>456886, "categories"=>["Chemistry"], "users"=>["Eriko Koshimizu", "Shintaro Imamura", "Jie Qi", "Jamal Toure", "Delgado M. Valdez Jr", "Christopher E. Carr", "Jun-ichi Hanai", "Shuji Kishi"], "doi"=>"https://dx.doi.org/10.1371/journal.pone.0017688.g001", "stats"=>{"downloads"=>1, "page_views"=>5, "likes"=>0}, "figshare_url"=>"https://figshare.com/articles/_Transgenic_expression_of_zebrafish_Progerin_lamin_A_916_37_and_prelamin_A_/456886", "title"=>"Transgenic expression of zebrafish Progerin/lamin A-Δ37 and prelamin A.", "pos_in_sequence"=>0, "defined_type"=>1, "published_date"=>"2011-03-30 01:54:46"}
  • {"files"=>["https://ndownloader.figshare.com/files/786642"], "description"=>"<p>(<b>A</b>) Western blot analysis of intrinsic lamin A/C in the zebrafish AB9 cells transfected with MOs. The lower panel of blotting shows the actin control (*<i>P</i><0.01). The right-side graph shows the quantitation results for the lamin A and C blot intensities standardized by the control actin levels from three-independent experiments. (<b>B</b>) Agarose gel electrophoresis of the RT-PCR products of zlamin A from embryos injected with the indicated concentrations of z<i>LMNA</i>-MO2. The primers used recognize exon 9 (forward primer; F-Primer) and the 3′-untranslated region (reverse primer; R-Primer). Sequence analysis revealed that the injection of z<i>LMNA</i>-MO2 induces a 24 bp deletion in the rear part of exon 11. Left panel, total RNA was extracted from 24 hpf embryos after MO injection. Right panel, embryos were injected with 8 ng MO and total RNA was extracted from 24 to 72 hpf as indicated. Lower panel, the corresponding positions of the F-Primer, R-Primer, and MO2 are schematically presented. (<b>C</b>) Gross morphology of zlamin A/C-knockdown embryos. Lateral views of MO-injected embryos (4 ng) at 24 hpf are shown. (a) 5-base mismatch control MO1 (MO1, 5-mis), (b) z<i>LMNA</i>-MO1 (MO1, MO), (c) 5-base mismatch control MO2 (MO2, 5-mis), (d) z<i>LMNA</i>-MO2 (MO2, MO). (<b>D</b>) Occasionally observed rough skin phenotypes (Mild and Severe) in MO2-morphant tails are shown by comparison with a normal skin phenotype (Normal) in the wild-type tail.</p>", "links"=>[], "tags"=>["zebrafish", "lamin"], "article_id"=>457011, "categories"=>["Chemistry"], "users"=>["Eriko Koshimizu", "Shintaro Imamura", "Jie Qi", "Jamal Toure", "Delgado M. Valdez Jr", "Christopher E. Carr", "Jun-ichi Hanai", "Shuji Kishi"], "doi"=>"https://dx.doi.org/10.1371/journal.pone.0017688.g002", "stats"=>{"downloads"=>1, "page_views"=>2, "likes"=>0}, "figshare_url"=>"https://figshare.com/articles/_Knockdown_of_zebrafish_lamin_A_C_/457011", "title"=>"Knockdown of zebrafish lamin A/C.", "pos_in_sequence"=>0, "defined_type"=>1, "published_date"=>"2011-03-30 01:56:51"}
  • {"files"=>["https://ndownloader.figshare.com/files/787178"], "description"=>"<p>Lateral view of 5 dpf larvae stained with Oil Red O. Strong staining can be observed around the head, the otic vesicle, the jaw, the swim bladder and the heart, as well as in the yolk of the Cont-MO-injected larvae. In contrast, in z<i>LMNA</i>-MOs-injected embryos, obvious defects in lipid deposits can be observed in all the tissues except the swim bladder. Duplicate samples are shown for each MO-injected specimen.</p>", "links"=>[], "tags"=>["lipodystrophic", "phenotype", "caused", "zebrafish", "lamin"], "article_id"=>457537, "categories"=>["Chemistry"], "users"=>["Eriko Koshimizu", "Shintaro Imamura", "Jie Qi", "Jamal Toure", "Delgado M. Valdez Jr", "Christopher E. Carr", "Jun-ichi Hanai", "Shuji Kishi"], "doi"=>"https://dx.doi.org/10.1371/journal.pone.0017688.g006", "stats"=>{"downloads"=>2, "page_views"=>6, "likes"=>0}, "figshare_url"=>"https://figshare.com/articles/_A_lipodystrophic_phenotype_is_caused_by_the_zebrafish_lamin_A_C_knockdown_/457537", "title"=>"A lipodystrophic phenotype is caused by the zebrafish lamin A/C knockdown.", "pos_in_sequence"=>0, "defined_type"=>1, "published_date"=>"2011-03-30 02:05:37"}
  • {"files"=>["https://ndownloader.figshare.com/files/787077"], "description"=>"<p>(<b>A</b>) Apoptosis and cell cycle analysis in 24 hpf embryos. (a–d) Lateral view of apoptotic phenotypes in MO-injected embryos using a TUNEL assay (TUNEL-positive cells are indicated by the red fluorescence spots). z<i>LMNA</i>-MO1-injected embryos shows increased apoptosis in the head and trunk. (e–h) BrdU incorporation in MO-injected embryos. z<i>LMNA</i>-MO2-injected embryos show increased BrdU-positive cells throughout the whole body. (i–l) MO-injected embryos stained with anti-phospho histone H3 (pH 3). A z<i>LMNA</i>-MO1-injected embryo shows a decreased number of pH 3-positive cells. Quantifications of the BrdU and pH 3 intensities in morphants are shown in right graphs (BrdU: MO1, <i>P</i><0.05 for 5-mis versus MO, MO2, <i>P</i><0.05 for 5-mis versus MO; pH 3: MO1, <i>P</i><0.05 for 5-mis versus MO, MO2, no significance for 5-mis versus MO). (<b>B</b>) Genes involved in the p53-related and cdk2 pathways were analyzed by semi-quantitative RT-PCR in MO-injected embryos at 24 hpf. Quantifications of the bands intensities for p21 are shown in the bottom graph (<i>P</i><0.01 for 5-mis versus MO in MO1 and MO2). (<b>C</b>) SA-β-gal assay of 6 dpf MO-injected larvae in comparison with each control 5-mis MO. Qualifications of the SA-β-gal activity are shown in bottom graph. The z<i>LMNA</i>-MO2-injected embryos revealed strong induction of SA-β-gal activity (<i>P</i><0.01 for 5-mis versus MO in MO2), whereas the z<i>LMNA</i>-MO1-injected embryos did not exhibit any obvious activity, compared with Cont-MO1-injected embryos.</p>", "links"=>[], "tags"=>["knockdown", "zebrafish", "lamin", "induces", "aberrant"], "article_id"=>457439, "categories"=>["Chemistry"], "users"=>["Eriko Koshimizu", "Shintaro Imamura", "Jie Qi", "Jamal Toure", "Delgado M. Valdez Jr", "Christopher E. Carr", "Jun-ichi Hanai", "Shuji Kishi"], "doi"=>"https://dx.doi.org/10.1371/journal.pone.0017688.g005", "stats"=>{"downloads"=>0, "page_views"=>0, "likes"=>0}, "figshare_url"=>"https://figshare.com/articles/_The_knockdown_of_zebrafish_lamin_A_C_induces_an_aberrant_cell_cycle_apoptosis_and_senescence_/457439", "title"=>"The knockdown of zebrafish lamin A/C induces an aberrant cell cycle, apoptosis, and senescence.", "pos_in_sequence"=>0, "defined_type"=>1, "published_date"=>"2011-03-30 02:03:59"}

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Relative Metric

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