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In JoVE (2)
- Model Genetik Organizma olarak kullanmak için Medaka Embriyolar, Mikroenjeksiyon
- Chimeras Üretim Medaka Embriyolar ve Hücre Nakli Dechorionation
Other Publications (2)
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Articles by Huijia Wang in JoVE
JoVE General
Model Genetik Organizma olarak kullanmak için Medaka Embriyolar, Mikroenjeksiyon
Centre for Regenerative Medicine, Department of Biology and Biochemistry, University of Bath
Medaka ve zebrafish omurgalı genomu fonksiyonları genetik diseksiyon için tamamlayıcı niteliktedir. Bu protokol, Medaka embriyolara başarılı mikroenjeksiyon, bir laboratuvarda Medaka ve zebrafish kullanarak embriyolojik ve genetik analiz için önemli bir tekniktir için kilit noktaları vurgulamaktadır.
JoVE General
Chimeras Üretim Medaka Embriyolar ve Hücre Nakli Dechorionation
Centre for Regenerative Medicine, Department of Biology and Biochemistry, University of Bath
, Sert koryon ve yumuşak embriyolar, Medaka embriyo manipülasyonu nedeniyle daha zebrafish içinde daha fazla yer almaktadır. Bu video görüntüleme ve kuruntulardan üretimi için hücre nakli için agaroz dechorionation montaj Medaka embriyolar işlemek için nasıl adım adım yordamlar, gösterir. Bu prosedürler, omurgalı genomu fonksiyonları genetik diseksiyon için tamamlayıcı özellikleri tam olarak yararlanmak için bir laboratuvar Medaka ve zebrafish kullanmak için gereklidir.
Other articles by Huijia Wang on PubMed
Essential Techniques for Introducing Medaka to a Zebrafish Laboratory--towards the Combined Use of Medaka and Zebrafish for Further Genetic Dissection of the Function of the Vertebrate Genome
The medaka, Oryzias latipes, a small egg-laying freshwater fish, is one of the three vertebrate model organisms in which genome-wide phenotype-driven mutant screens have been carried out. Despite a number of large-scale screens in zebrafish, a substantial number of mutants with new distinct phenotypes were identified in similar large-scale screens in the medaka. This observed difference in phenotype is due to the two species having a unique combination of genetic, biological and evolutional properties. The two genetic models share a whole-genome duplication event over that of tetrapods; however, each has independently specialized or lost the function of one of the two paralogues. The two fish species complement each other as genetic systems as straightforward comparison of phenotypes, ease of side-by-side analysis using the same techniques and simple and inexpensive husbandry of mutants make these small teleosts quite powerful in combination. Furthermore, both have draft genome sequences and bioinformatic tools available that facilitate further genetic dissection including whole-genome approaches. Together with the gene-driven approach to generate gene knockout mutants of the fish models, the two fish models complement the mouse in genetically dissecting vertebrate genome functions. The external embryogenesis and transparent embryos of the fish allow systematic isolation of embryonic lethal mutations, the most difficult targets in mammalian mutant screens. This chapter will describe how to work with both medaka and zebrafish almost as one species in a lab, focusing on medaka and highlighting the differences between the medaka and zebrafish systems.
Insufficiency of BUBR1, a Mitotic Spindle Checkpoint Regulator, Causes Impaired Ciliogenesis in Vertebrates
Budding uninhibited by benzimidazole-related 1 (BUBR1) is a central molecule of the spindle assembly checkpoint. Germline mutations in the budding uninhibited by benzimidazoles 1 homolog beta gene encoding BUBR1 cause premature chromatid separation (mosaic variegated aneuploidy) [PCS (MVA)] syndrome, which is characterized by constitutional aneuploidy and a high risk of childhood cancer. Patients with the syndrome often develop Dandy-Walker complex and polycystic kidneys; implying a critical role of BUBR1 in morphogenesis. However, little is known about the function of BUBR1 other than mitotic control. Here, we report that BUBR1 is essential for the primary cilium formation, and that the PCS (MVA) syndrome is thus a novel ciliopathy. Morpholino knockdown of bubr1 in medaka fish also caused ciliary dysfunction characterized by defects in cerebellar development and perturbed left-right asymmetry of the embryo. Biochemical analyses demonstrated that BUBR1 is required for ubiquitin-mediated proteasomal degradation of cell division cycle protein 20 in the G0 phase and maintains anaphase-promoting complex/cyclosome-CDC20 homolog 1 activity that regulates the optimal level of dishevelled for ciliogenesis.
