Zebrafish dou yan mutation causes patterning defects and extensive cell death in the retina

Abstract

The size of an organ is largely determined by the number of cells it contains, which in turn is regulated by two opposing processes, cell proliferation and cell death, however, it is generally not clear how cell proliferation and cell death are coordinated during development. Here, we characterize the zebrafish dou yan mi234 mutation that results in a dramatic reduction of retinal size and a disruption of retinal differentiation and lamination. The retinal size reduction is caused by increased retinal cell death in a non-cell-autonomous manner during early development. The phenotypic defect in dou yan mi234 arises coincident with the onset of retinal neurogenesis and differentiation. Interestingly, unlike many other small eye mutations, the mutation does not increase the level of cell death in the brain, suggesting that the brain and retina use different mechanisms to maintain cell survival. Identification and further study of the dou yan gene will enhance our understanding of the molecular mechanisms regulating retinal cellular homeostasis, i.e., the balance between cell proliferation and cell death. Developmental Dynamics 236: 1295-1306, 2007.

Intact Retinal Pigment Epithelium Maintained by Nok Is Essential for Retinal Epithelial Polarity and Cellular Patterning in Zebrafish

“…To visualize donor cells, we first generated a stable transgenic fish line (pt104) that expresses GFP under the ubiquitous EF1α promoter in a wildtype genetic background. The transgenic GFP expression allows a visualization of live donor cells, avoiding the signal interference from dead donor cells when labeled with conventional non-degradable dextran conjugates (Catalano et al, 2007). We found the apical markers Nok and ZO-1 of the wildtype pt104 donor cells localized apically in pt106 host retinas but internally in nok m520 host retinas (Fig.…”

Chemical genetic effects of Sargassum wightii during embryonic development in zebrafish

“…Figure 2b shows the phenocopies of the reduction in the eye size in the embryo which is evident as dou yan genetic mutation. [ 16 ] Tubular heart phenotype was observed in the CF treated embryos and a failure of the myocardium thickening was noticed in the developing embryo as like the heart of glass ( heg ) mutant and shown in Figure 2d and e , resulting the decrease of HBR with pericardial bulging and tubular heart.…”

Characterization of Zebrafish Pax1b and Pax9 in Fin Bud Development

“…The size of an organ is largely determined by the number of cells it contains and cell death is an essential aspect in this process [ 28 ]. The phenotype of fin bud defects in pax1b morphants might have a close relationship with cell death.…”