Novel Function of ADP-Ribosylation Factor-like 6 Interacting Protein in the Ocular Development of Zebrafish Embryos
Date Issued
2008
Date
2008
Author(s)
Liu, Jeng-Ting
Abstract
ADP-ribosylation factor-like 6 interacting protein (Arl6ip) was a maternally inherited gene in zebrafish, and it was expressed throughout the whole embryo before the gastrula period and restrictedly expressed in certain tissues after the pharyngula period. As losing Arl6ip, many phenotypic defects occurred in many tissues of the zebrafish embryo, such as brain, eyes, heart, and trunk. In particular, the occurrence of microphthalmos of eye and incomplete differentiation of retina were found. According to previous researches, Arl6ip was thought closely related to cell differentiation, but its biological function in development was unknow. Here we confer the molecular mechanism that Arl6ip involved in by observing the expression of related genes releated to zeberfish eyes development. First, we found that the expressions of early patterning genes were affected while losing Arl6ip, including overexpression of shh mRNA in the head, down-regulated of rx1 and pax6 mRNA in the eye field, and elevated expression of pax2 mRNA in optic stalk. These change in gene expression all result in the reduction of eye field. Then, we focued on the expressions of specific genes as retinal development. As losing Arl6ip, zebrafish embryos could not express shh, six3a, and six6 normally; that affected the differentiating processes of retina progenitor. Therefore, we could observe the specific proteins such as HuC, Neurolin, and HNK-1 were repressed in retina, and the photoreceptor specific gene crx was crowded at the ventral site of eyes. Furthermore, we labeled the cells in the eye field with deltaC and confirmed the cell fate of retinal progenitor kept indetermination while losing Arl6ip. Finally, we examined the level of cell proliferation in the eye field. While losing Arl6ip, we could observe the BrdU signals were higher in the eye, and the retinal progenitor kept expressing cyclin D1 but not p57kip2, suggesting the eye progenitor cell stayed as an early progenitor and could not exit cell cycle to process differentiation. Thus, inhibition of Arl6ip leads to arrest eye development at the early stage. These mal-functional eye progenitors keep proliferating and continually express early marker gene. Taken together, we conclude that arl6ip not only affects the signals controlling eye development, but also plays an important role in cell differentiation.
Subjects
zebrafish
eye
development
File(s)![Thumbnail Image]()
Loading...
Name
ntu-97-R95b43016-1.pdf
Size
23.32 KB
Format
Adobe PDF
Checksum
(MD5):17cb1b1a429f6bd43c3a5e0ad589d896