Loss of selenoprotein N function causes disruption of muscle architecture in the zebrafish embryo

Deniziak, Marzanna; Thisse, Christine; Rederstorff, Mathieu; Hindelang, C.; Thisse, Bernard; Lescure, Alain

doi:10.1016/j.yexcr.2006.10.005

Cited by 87 publications

(77 citation statements)

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“…The homogenate was centrifuged at 9000 × g for 5 min at 4 o C. The supernatant, containing the enzyme, was reacted with H 2 O 2 for 1 min at 37 o C. The reaction was stopped with 32.4 mmol/L ammonium molybdate, and the enzyme activity measured at 405 nm with a UV-Vis spectrophotometer (UV-1601PC, Shimadzu, Japan). The expression of the sepn1 gene in wild-type zebrafish was assessed by RT-PCR performed on total RNA samples isolated from 72 hpf flies (n = 30), using a modification to the method described by Deniziak et al 12 Total RNA was obtained using the easy-BLUE™ Total RNA Extraction Kit (iNtRON Biotechnology, Inc.) according to the manufacturer's instruction. Reverse transcription was performed using 8 u of a One-…”

Section: Methodsmentioning

confidence: 99%

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Effects of Nanometer Sized Silver Materials on Biological Toxicity During Zebrafish Embryogenesis

Yeo¹,

Kang

2008

Bulletin of the Korean Chemical Society

101

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Commercial nanometer sized silver is widely used for its antibacterial effect; however, nanoparticles may also have ecotoxicological effects after being discharged into water. Nanometer sized silver can flow into aquatic environments, where it can exert a variety of physiologically effects in living organisms, including fish. The present study aimed to investigate the effect of nanometer sized silver on the development of zebrafish embryos, analyze the properties of commercial nanometer sized silver and define the toxicity relationship between embryogenesis and hatched flies. The commercial nanometer sized silver was analyzed in the Ag + ion form. The hatch rate decreased in the nano-silver exposed groups (10 and 20 ppt); furthermore, the hatched flies had an abnormal notochord, weak heart beat, damaged eyes and curved tail. The expression of the Sel N1 gene decreased in the nano-silver exposed groups, and the catalase activities of the exposed groups increased relative to those in the control group. Therefore, the Ag + ions in commercial nanometer sized silver could accumulate in aquatic environments and seriously damage the development of zebrafish embryos.

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Section: Methodsmentioning

confidence: 99%

“…Selenoprotein N1 (Sel N1) is related to vertebra development, as well as heart disease in zebrafish. 12 The relationship of the Sel N1 gene with nanosilver was also investigated. Moreover, the anti-oxide effects were investigated with regard to the catalase (EC: 1.11.16) activity.…”

Section: Introductionmentioning

confidence: 99%

Effects of Nanometer Sized Silver Materials on Biological Toxicity During Zebrafish Embryogenesis

Yeo¹,

Kang

2008

Bulletin of the Korean Chemical Society

101

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“…SelN is an ER-resident transmembrane glycoprotein that is highly expressed during embryonic development and to a lesser extent in adult tissues including skeletal muscle (286). Recent studies using a zebrafish animal model revealed that SelN is required for early muscle development and differentiation in this organism (77,165). More recently, SelN Ϫ/Ϫ mice were developed (50,293).…”

Section: K Selenoprotein Nmentioning

confidence: 99%

Selenoproteins: Molecular Pathways and Physiological Roles

Labunskyy

Hatfield

Gladyshev³

2014

Physiological Reviews

994

835

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Selenium is an essential micronutrient with important functions in human health and relevance to several pathophysiological conditions. The biological effects of selenium are largely mediated by selenium-containing proteins (selenoproteins) that are present in all three domains of life. Although selenoproteins represent diverse molecular pathways and biological functions, all these proteins contain at least one selenocysteine (Sec), a seleniumcontaining amino acid, and most serve oxidoreductase functions. Sec is cotranslationally inserted into nascent polypeptide chains in response to the UGA codon, whose normal function is to terminate translation. To decode UGA as Sec, organisms evolved the Sec insertion machinery that allows incorporation of this amino acid at specific UGA codons in a process requiring a cis-acting Sec insertion sequence (SECIS) element. Although the basic mechanisms of Sec synthesis and insertion into proteins in both prokaryotes and eukaryotes have been studied in great detail, the identity and functions of many selenoproteins remain largely unknown. In the last decade, there has been significant progress in characterizing selenoproteins and selenoproteomes and understanding their physiological functions. We discuss current knowledge about how these unique proteins perform their functions at the molecular level and highlight new insights into the roles that selenoproteins play in human health.

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“…Although it is not a muscle specific protein and it is ubiquitously expressed, its expression is particularly marked in cultured myoblasts and decreases in differentiating myotubes, suggesting a role in early development and in cell proliferation and regeneration 186 . In zebrafish embryos deficient for sePN, muscle organization and myofibrils architecture are altered during early development 187 .…”

Section: Therapeutic Perspectivesmentioning

confidence: 99%

Congenital muscular dystrophy. Part II: a review of pathogenesis and therapeutic perspectives

Reed

2009

Arq. Neuro-Psiquiatr.

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-The congenital muscular dystrophies (CMDs) are a group of genetically and clinically heterogeneous hereditary myopathies with preferentially autosomal recessive inheritance, that are characterized by congenital hypotonia, delayed motor development and early onset of progressive muscle weakness associated with dystrophic pattern on muscle biopsy. The clinical course is broadly variable and can comprise the involvement of the brain and eyes. From 1994, a great development in the knowledge of the molecular basis has occurred and the classification of CMDs has to be continuously up dated. In the last number of this journal, we presented the main clinical and diagnostic data concerning the different subtypes of CMD. In this second part of the review, we analyse the main reports from the literature concerning the pathogenesis and the therapeutic perspectives of the most common subtypes of CMD: MDC1A with merosin deficiency, collagen VI related CMDs (Ullrich and Bethlem), CMDs with abnormal glycosylation of alpha-dystroglycan (Fukuyama CMD, Muscleeye-brain disease, Walker Warburg syndrome, MDC1C, MDC1D), and rigid spine syndrome, another much rare subtype of CMDs not related with the dystrophin/glycoproteins/extracellular matrix complex.Key WorDs: congenital muscular dystrophy, MDC1A, collagen VI related disorders, glycosylation of alphadystroglycan, Fukuyama DMC, muscle-eye-brain (MeB) disease, Walker-Warburg syndrome, rigid spine syndrome. distrofia muscular congênita. parte ii: revisão da patogênese e perspectivas terapêuticas resumo -As distrofias musculares congênitas (DMCs) são miopatias hereditárias geralmente, porém não exclusivamente, de herança autossômica recessiva, que apresentam grande heterogeneidade genética e clínica. são caracterizadas por hipotonia muscular congênita, atraso do desenvolvimento motor e fraqueza muscular de início precoce associada a padrão distrófico na biópsia muscular. o quadro clínico, de gravidade variável, pode também incluir anormalidades oculares e do sistema nervoso central. A partir de 1994, os conhecimentos sobre genética e biologia molecular das DMCs progrediram rapidamente, sendo a classificação continuamente atualizada. os aspectos clínicos e diagnósticos dos principais subtipos de DMC foram apresentados no número anterior deste periódico, como primeira parte desta revisão. Nesta segunda parte apresentaremos os principais mecanismos patogênicos e as perspectivas terapêuticas dos subtipos mais comuns de DMC: DMC tipo 1A com deficiência de merosina, DMCs relacionadas com alterações do colágeno VI (Ullrich e Bethlem), e DMCs com anormalidades de glicosilação da alfa-distroglicana (DMC Fukuyama, DMC "Muscle-eye-brain" ou MeB, síndrome de Walker Warburg, DMC tipo 1C, DMC tipo 1D). A DMC com espinha rígida, mais rara e não relacionada com alterações do complexo distrofina-glicoproteínas associadas-matriz extracelular também será abordada quanto aos mesmos aspectos patogênicos e terapêuticos.PAlAVrAs-ChAVes: distrofia muscular congênita, merosina, colágeno VI, glicosila...

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Loss of selenoprotein N function causes disruption of muscle architecture in the zebrafish embryo

Cited by 87 publications

References 50 publications

Effects of Nanometer Sized Silver Materials on Biological Toxicity During Zebrafish Embryogenesis

Effects of Nanometer Sized Silver Materials on Biological Toxicity During Zebrafish Embryogenesis

Selenoproteins: Molecular Pathways and Physiological Roles

Congenital muscular dystrophy. Part II: a review of pathogenesis and therapeutic perspectives

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