<i>dino</i> and <i>mercedes</i>, two genes regulating dorsal development in the zebrafish embryo

Hammerschmidt, M.; Pelegri, Francisco; Mullins, Mary C.; Kane, Donald A.; Eeden, Freek van; Granato, Michael; Brand, Michael; Furutani-Seiki, Makoto; Haffter, P.; Heisenberg, Carl‐Philipp; Jiang, Yun-Jin; Kelsh, R. N.; Odenthal, J.; Warga, Rachel M.; Nüsslein‐Volhard, Christiane

doi:10.1242/dev.123.1.95

Cited by 304 publications

(42 citation statements)

References 46 publications

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“…We therefore investigated cell death in associated with the LMFF reduction. First, we performed acridine orange staining, which is used to identify cell death in living specimens 28 , 29 , at the LMFF-reducing stage (6.0–6.5 mm SL, n = 6; 6.5–7.0 mm SL, n = 6; 7.0–7.5 mm SL, n = 5) (Fig. 2 a–c”).…”

Section: Resultsmentioning

confidence: 99%

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Developmental independence of median fins from the larval fin fold revises their evolutionary origin

Miyamoto

Kawakami

Tamura

et al. 2022

Sci Rep

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The median fins of modern fish that show discrete forms (dorsal, anal, and caudal fins) are derived from a continuous fold-like structure, both in ontogeny and phylogeny. The median fin fold (MFF) hypothesis assumes that the median fins evolved by reducing some positions in the continuous fin fold of basal chordates, based on the classical morphological observation of developmental reduction in the larval fin folds of living fish. However, the developmental processes of median fins are still unclear at the cellular and molecular levels. Here, we describe the transition from the larval fin fold into the median fins in zebrafish at the cellular and molecular developmental level. We demonstrate that reduction does not play a role in the emergence of the dorsal fin primordium. Instead, the reduction occurs along with body growth after primordium formation, rather than through actively scrapping the non-fin forming region by inducing cell death. We also report that the emergence of specific mesenchymal cells and their proliferation promote dorsal fin primordium formation. Based on these results, we propose a revised hypothesis for median fin evolution in which the acquisition of de novo developmental mechanisms is a crucial evolutionary component of the discrete forms of median fins.

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Section: Resultsmentioning

confidence: 99%

“…Acridine orange (AO; #A6014-10G, Sigma) was used to identify cell death including apoptosis 28 , 29 following the method of Freitas et al 27 . Embryos were incubated in the dark in 0.5 μg/ml AO in PBS at room temperature for 30 min and rinsed three times in fish water for 10 min.…”

Section: Methodsmentioning

confidence: 99%

Developmental independence of median fins from the larval fin fold revises their evolutionary origin

Miyamoto

Kawakami

Tamura

et al. 2022

Sci Rep

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“…Understanding various forms of apoptosis could be the key to unlocking the diagnosis and therapy of the related diseases. Several methods such as fluorescent nucleic binding dyes, i.e., acridine orange, 16 ethidium bromide, 16 and propidium bromide 17 along with standard methods like terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL staining) based on end labeling of enzymatic DNA degradation products exist for labelling apoptotic cells in vitro. 18 There exist few other approaches for labelling apoptotic cells in vivo.…”

Section: Introductionmentioning

confidence: 99%

Photoluminescent graphene quantum dots for in vivo imaging of apoptotic cells

et al. 2015

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Apoptosis (programmed cell death) is linked to many incurable neurodegenerative, cardiovascular and cancer causing diseases. Numerous methods have been developed for imaging apoptotic cells in vitro; however, there are few methods available for imaging apoptotic cells in live animals (in vivo). Here we report a novel method utilizing the unique photoluminescence properties of plant leaf-derived graphene quantum dots (GQDs) modified with annexin V antibody (AbA5) to form (AbA5)-modified GQDs (AbA5-GQDs) enabling us to label apoptotic cells in live zebrafish (Danio rerio). The key is that zebrafish shows bright red photoluminescence in the presence of apoptotic cells. The toxicity of the GQDs has also been investigated with the GQDs exhibiting high biocompatibility as they were excreted from the zebrafish's body without affecting its growth significantly at a concentration lower than 2 mg mL(-1) over a period of 4 to 72 hour post fertilization. The GQDs have further been used to image human breast adenocarcinoma cell line (MCF-7 cells), human cervical cancer cell line (HeLa cells), and normal human mammary epithelial cell line (MCF-10A). These results are indispensable to further the advance of graphene-based nanomaterials for biomedical applications.

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“…digoxigenin, Roche Diagnostics). runx1 , 30 spi1b 31 and gata1a 32 probes were synthesized according to literature. To detect haemoglobin activity, o ‐dianisidine (Sigma) staining was performed as described in Ref.…”

Section: Methodsmentioning

confidence: 99%

Dysregulation of NIPBL leads to impaired RUNX1 expression and haematopoietic defects

Mazzola

Pezzotta

Fazio

et al. 2020

J Cellular Molecular Medi

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The transcription factor RUNX1, a pivotal regulator of HSCs and haematopoiesis, is a frequent target of chromosomal translocations, point mutations or altered gene/protein dosage. These modifications lead or contribute to the development of myelodysplasia, leukaemia or platelet disorders. A better understanding of how regulatory elements contribute to fine‐tune the RUNX1 expression in haematopoietic tissues could improve our knowledge of the mechanisms responsible for normal haematopoiesis and malignancy insurgence. The cohesin RAD21 was reported to be a regulator of RUNX1 expression in the human myeloid HL60 cell line and during primitive haematopoiesis in zebrafish. In our study, we demonstrate that another cohesin, NIPBL, exerts positive regulation of RUNX1 in three different contexts in which RUNX1 displays important functions: in megakaryocytes derived from healthy donors, in bone marrow samples obtained from adult patients with acute myeloid leukaemia and during zebrafish haematopoiesis. In this model, we demonstrate that alterations in the zebrafish orthologue nipblb reduce runx1 expression with consequent defects in its erythroid and myeloid targets such as gata1a and spi1b in an opposite way to rad21. Thus, also in the absence of RUNX1 translocation or mutations, additional factors such as defects in the expression of NIPBL might induce haematological diseases.

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dino and mercedes, two genes regulating dorsal development in the zebrafish embryo

Cited by 304 publications

References 46 publications

Developmental independence of median fins from the larval fin fold revises their evolutionary origin

Developmental independence of median fins from the larval fin fold revises their evolutionary origin

Photoluminescent graphene quantum dots for in vivo imaging of apoptotic cells

Dysregulation of NIPBL leads to impaired RUNX1 expression and haematopoietic defects

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